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Right  innominate  vein 
Left  innominate  vein 
Sniieriot  vena  cava 
Vena  azygos 
Pulmonary  vein 


Innominate  artery 


Left  common  carotid  artery 

Left  subclavian  artery 


Left  internal  jugular  vein 


Stump  of  sup.  cava 
R.  auricular  append. 

Aorta 

Left  coronary  artery 

Right  coronary  vessels 

Riglit  nutrginal  artery 


Ri;;ht  ventricle 


Left  pulmonary  artery 


Superior  pulmo- 
nary vein 


Inferior  pulmo- 
nary vein 


t.eft  auricular 
appendage 
Conus  anteriorsus 
Interventricular  branches 
of  left  coronary  vessels 
Left  ventricle 


Fio.  1. — The  lieart  and  great  vessels,  viewed  fru 


jnt.     (After  Piersol.) 


Left  pulmonary  artery"" 


Superior  left  pulmonary  vein. 

Inferior  left  pulmonary  vein 
Termination  of  left  coronary^ 
vein 
Transverse  brancii  of  left 
coronary  artery 


Left  ventricle 


Superior  vena  cava 

Superior  right  pulmonary  vein 
Right  pulmonary  artery 

Inferior  right  pulmonary  vein 


Inferior  vena  cava 


Coronary  sinus 

Right  coronary  vein 
Transverse  branch  of  right 

coronary  artery 
Posterior  descending  branch  of 

right  coronary  artery 


— -Middle  cardiac  vein 


Right  ventricle 


Fio.  2. — Same,  irom  behind.     (After  Piersol.) 


L^ 


DISEASES 


of  the 


HEART  AND  AORTA 


BY 

ARTHUR   DOUGLASS  HIRSCHFELDER,  M.D. 

ASSOCIATE   IN   MEDICINE,   JOHNS   HOPKINS   UNIVERSITY 

WITH   AN  INTRODUCTORY  NOTE 
BY 

LEWELLYS    F.  BARKER,  M.D.,  LL.D. 

PROFESSOR   OP   MEDICINE,   JOHNS   HOPKINS   UNIVERSITY 


j^9  ILLUSTRATIONS  BT  THE  AUTHOR 


PHILADELPHIA  ^  LONDON 

J.  B.  LIPPINCOTT    COMPANY 


COPYHIGHT,  1910 

By  J.  B.  LippiNCOTT  Company 


Printed  by  J.  B.  Lippincott  Company 
The  Washington  Square  Press,  Philadelphia,  U.  S.  A. 


TO 

MY  FATHER 

I'rofessor  of  Clinical  Medicine,  Leland  Stanford  Junior  University 
AND    TO 

Professor  of  Medicine,  Johns  Hopkins  University 

CHIEFS    OF    THE    CLINICS    IN    WHICH    THE    WORK    WAS    DONE;    WHO 

HAVE   TAUGHT   ME    BY   PRECEPT   AND    EXAMPLE   HOW 

SCIENCE,  ART,  AND    HUMANITY    SHOULD 

BE    WOVEN    INTO    PRACTICE 

OF    MEDICINE 

THIS  BOOK  IS  AFFECTIONATELY  DEDICATED 


INTRODUCTORY   NOTE 


The  researches  in  the  great  field  of  inner  medicine  have  so  multiplied 
in  recent  years  that  it  has  become  highly  desirable  that  we  should  have 
from  time  to  time,  in  addition  to  the  summaries  of  progress  contained 
in  the  general  text-books  on  practice,  monographs  which  picture  more 
completely  the  status  of  our  knowledge  in  the  several  special  divisions 
of  the  subject.  In  diseases  of  the  circulatory  system  new  methods  of 
study  have  led  to  the  discovery  of  many  new  facts,  and  a  great  many 
workers  have  been  attracted  during  the  last  twenty  years  to  this  domain 
of  cardiovascular  inquiry. 

In  the  medical  clinic  at  the  Johns  Hopkins  Hospital,  Dr.  Hirsch- 
felder  has  during  the  past  few  years  occupied  himself  especially  with 
such  studies.  The  present  volume  is  an  attempt  to  epitomize  the  actual 
condition  of  the  subject  at  the  present  time,  as  viewed  from  the  stand- 
point of  an  active  investigator  of  extensive  first-hand  experience  who 
has  also  a  wide  acquaintance  with  the  literature  of  the  physiology  and 
pathology  of  the  circulatory  apparatus. 

The  clearness  and  brevity  of  the  presentation  and  the  excellent 
arrangement  of  the  material  will,  I  am  sure,  appeal  to  students  and 
practitioners  of  medicine.  It  is  no  easy  matter  adequately  to  combine 
the  most  recent  results  of  anatomical,  physiological,  pathological,  and 
clinical  studies  in  a  form  which  will  satisfy  the  critical  demands  of  the 
scientific  investigator  and  at  the  same  time  be  useful  as  a  guide  to 
the  every-day  practitioner.  Especial  attention  has  been  paid  in  the 
volume  to  the  practical  facts  of  diagnosis  and  treatment;  in  the  more 
theoretical  portions  there  will  be  found  evidence  of  careful,  critical 
sifting,  and  an  appreciation  of  the  distinction  between  what  is  essential 
and  what  non-essential  for  the  more  general  reader. 

The  bibliographic  references  make  no  attempt  at  completeness,  but 
have  been  chosen  with  the  idea  in  mind  of  permitting  those  who  desire 
to  do  so  to  consult  the  most  important,  and  especially  the  more  recent, 
treatises,  monographs,  and  original  articles  which  deal  with  the  various 
matters  discussed. 

A  notable  feature  of  Dr.  Hirschfelder's  book  is  the  liberality  of  illus- 
trations; the  majority  of  the  figures  are  made  from  original  drawings 
and  tracings  and  are  in  pleasing  contrast  with  the  time-worn  figures 
which  pass  from  compilation  to  compilation. 

Lewellys  F.  Barker. 
Baltimore,  May  12,  1910. 

V 


PREFACE 


In  the  preparation  of  this  book  it  has  been  the  writer's  aim  to  present 
side  by  side  the  phenomena  observed  at  the  bedside  and  the  facts  learned 
in  the  laboratory  in  order  to  show  how  each  supplements  the  other  in 
teaching  us  how  to  observe  the  patient  and  to  direct  the  treatment.  Many 
of  the  results  obtained  in  the  laboratory  have  not  yet  attained  practical 
importance  because  they  have  been  scattered  through  the  Uterature  and 
have  not  reached  the  eye  of  the  cUnician;  but  wherever  the  clinicians  have 
looked  to  the  laboratory  or  laboratory  workers  have  looked  to  the  clinic 
for  verification  or  application  of  their  theories  the  great  pillars  of  progress 
have  been  raised.  In  accordance  with  this  idea  the  clinical  presentation 
in  each  chapter  is  preceded  by  an  introductory  section  dealing  with  the 
experimental  pathology  and  more  fundamental  principles  of  the  subject, 
which  has  been  used  as  a  basis  for  frequent  reference  in  the  clinical  dis- 
cussions. 

The  trend  of  chnical  observation  during  the  past  two  decades  has  been 
toward  more  accurate  study  of  disturbances  of  function  and  toward  the 
introduction  of  mechanical  methods  for  their  observation,  methods  of 
precision  which  tend  to  supplement  or  supplant  the  older  and  simpler 
methods  of  physical  diagnosis.  Chief  among  these  may  be  mentioned  the 
study  of  blood-pressure,  the  graphic  studies  upon  alterations  in  cardiac 
rhythm  by  means  of  the  venous  pulse,  the  outlining  of  the  heart  and  vessels 
by  means  of  the  X-ray,  and  the  phonographic  recording  of  the  heart  sounds. 
Each  of  these  subjects  has  been  reviewed  with  special  reference  to  the 
general  principles  upon  which  the  method  is  based,  in  order  to  point  out 
its  applicability,  its  limitations,  the  character  of  information  which  it  has 
yielded  in  clinical  conditions,  the  conditions  under  which  the  same  informa- 
tion may  be  gained  by  simpler  methods,  the  conditions  under  which  its 
employment  is  essential  and  those  under  which  it  is  superfluous. 

The  failure  of  the  heart  has  been  traced  through  its  varying  stages 
from  the  simple  fatigue  of  the  normal  heart  in  exercise,  through  the  stage 
of  primary  overstrain,  to  that  of  broken  compensation,  especial  attention 
being  devoted  to  the  states  of  broken  pulmonary  compensation  arising 
from  failure  of  the  left  ventricle  and  of  broken  systemic  compensation 
from  failure  of  the  right. 


viii  PREFACE. 

The  pathogenesis  of  cardiac  symptoms  is  fully  discussed,  with  their 
pathological  physiology,  occurrence,  and  the  symptomatic  treatment  for 
their  reUef. 

The  general  methods  of  treatment  in  cardiac  diseases,  dietetic,  phar- 
macological, gymnastic,  hydrotherapeutic,  and  electrical,  have  been  treated 
both  as  empirical  procedures  and  as  experimental  methods  to  correct 
definite  disturbances  in  the  physiology  of  the  circulation,  especially  changes 
in  cardiac  force,  cardiac  tonicity,  and  peripheral  resistance. 

The  chapters  upon  the  individual  organic  lesions  include  discussions 
of  pathological  anatomy,  pathogenesis,  pathological  physiology,  as  well 
as  of  symptomatology,  course,  notes  of  typical  cases,  diagnosis,  treatment, 
and  prognosis.  Considerable  attention  is  also  paid  to  functional  disturb- 
ances (valvular  insufficiencies,  etc.)  which  may  bring  about  conditions 
similar  to  those  resulting  from  organic  changes  or  may  accompany  the 
latter.  The  Adams-Stokes  syndrome  seems  so  definitely  associated  with 
lesions  of  the  auriculoventricular  muscle  bundles  as  to  justify  its  classifi- 
cation among  conditions  due  to  organic  lesions. 

The  congenital  heart  lesions  are  viewed  as  disturbances  in  embryologic 
development  in  which  primary  malformations  or  states  in  fetal  life  have 
diverted  the  blood  current,  modifying  the  further  course  of  development 
and  producing  concomitant  secondary  malformations.  The  effect  of  these 
lesions  upon  the  adult  circulation  and  their  relation  to  cardiac  overstrain 
in  producing  the  syndrome  of  the  morbus  coeruleus  are  discussed,  as  well 
as  the  signs,  diagnosis,  prognosis,  and  treatment. 

Short  chapters  are  devoted  to  the  subjects  of  pregnancy  in  heart 
disease  and  the  effects  of  trauma  and  wounds  of  the  heart. 

Considerable  space  is  given  to  the  purely  functional  disturbances  of 
cardiac  action,  especially  to  the  physiological  mechanisms  by  which  many 
of  them  result  from  disturbances  in  distant  organs  as  well  as  to  the  improve- 
ments resulting  when  these  disturbances  are  corrected. 

A  great  deal  of  care  has  been  bestowed  by  the  writer  in  the  prepara- 
tion of  the  illustrations,  especially  upon  the  cardiosphygmographic  trac- 
ings, the  diagrammatic  representations  of  clinical  conditions  and  of  effects 
upon  the  blood  flow  in  different  parts  of  the  circulation  as  well  as  in  differ- 
ent stages  of  the  disease.  When  necessary,  figures  have  been  borrowed 
from  other  sources,  to  whom  due  credit  has  been  given. 

Since  the  aim  of  the  book  is  not  only  to  present  the  principal  facts 
but  to  aid  the  reader  in  following  out  lines  in  which  he  is  especially  inter- 
ested, an  adequate  bibliography  has  been  added  to  each  chapter,  embrac- 
ing the  articles  referred  to  in  the  text. 

It  is  a  pleasant  duty  for  the  writer,  in  conclusion,  to  express  his  thanks 
to  Professors  Barker  and  Thayer  for  the  privilege  of  using  the  clinical 


PREFACE.  ix 

material  and  records  of  the  Johns  Hopkins  Hospital,  to  Professor  T.  B. 
Futcher  for  that  of  the  Johns  Hopkins  Dispensary,  and  to  his  father.  Pro- 
fessor J.  O.  Hirschfelder,  for  the  cases  at  the  City  and  County  Hospital 
of  San  Francisco;  to  Professor  F.  P.  Mall  and  Drs.  Knower,  Retzer,  and 
Evans  in  matters  of  anatomy  and  embryology;  to  Professors  W.  H.  Howell, 
J.  Loeb,  and  Dr.  D.  R.  Hooker  in  physiology;  to  Professors  W.  S.  Hal- 
sted,  T.  S.  Cullen,  and  J.  M.  Slemons  in  matters  of  surgery,  gynaecology, 
and  obstetrics;  to  Professors  W.  G.  MacCallum  and  W.  Ophiils,  as  well 
as  to  Major  F.  F.  Russell,  Dr.  Lamb,  and  Dr.  Gray,  of  the  Army  Medical 
Museum,  for  the  use  of  pathological  material;  to  Professor  C.  M.  Cooper 
for  the  collection  of  radiographs;  to  Dr.  Chas.  S.  Bond  for  his  untiring 
labors  in  the  preparation  of  photomicrographs;  to  Professor  W.  Einthoven 
of  Leyden  for  the  use  of  electrocardiograms;  to  Professor  Max  Broedel 
for  his  kind  instruction  and  suggestions  in  matters  of  illustration;  to  Dr. 
Carohne  B.  Towles  for  her  assistance  in  reading  of  proof  as  well  as  for 
many  helpful  suggestions;  and  to  Miss  Alberta  E.  Bush  for  her  care  in  the 
technical  i^atters  pertaining  to  the  manuscript  and  index. 


CONTENTS 


PART  I. 
GENERAL  CONSIDERATIONS  AND  METHODS  OF  DIAGNOSIS. 

PAGE 

I.     Physiological  Considerations 1 

II.     Blood-pressure  and  Blood  Viscosity 18 

III.  The  Arterial  Pulse 41 

IV.  The  Venous  Pulse  and  Electrocardiogram  in  Health  and  Disease  . .  49 
V.     X-Ray  Examination 82 

VI.     Physical  Examination 88 

PART  11. 
DISEASED  CONDITIONS  DUE  TO  DIFFUSE  PATHOLOGICAL  PROCESSES. 

I.     Primary  Cardiac  Overstrain 121 

II.  Pathological    Physiology  ^f    Exercise,    Cardiac    Overstrain,    Heart 

Failure,  and  Broken  Compensation 129 

TIL    Symptoms  of  Cardiac  Disease 147 

IV.     General  Principles  of  Treatment  of  Failure  of  the  Heart 163 

V.    The  Effects  of  Drugs  in  Cardiac  Disease 172 

VI.     Gymnastics  and  Hydrotherapy 193 

VII.    Hypertrophy  and  Atrophy 203 

VIII.     Fatty  Deposits  in  and  about  the  Heart 214 

IX.     Affections  of  the  Myocardium 224 

X.     Arteriosclerosis 249 

XT.    Vasomotor  Crises,  etc.,  and  thh  Angioneurotic  Lesions 270 

XII.    Sclerosis  of  the  Coronary  Arteries,  and  Angina  Pectoris 280 

PART  III. 

DISEASED  CONDITIONS  DUE  TO  LOCALIZED  LESIONS. 

I.  Endocarditis 299 

II.  Mitral  Insufficiency 321 

III.  Mitral  Stenosis 341 

rV.  Aortic  Insufficiency 360 

V.  Aortic  Stenosis 381 

VI.  Pulmonary'  Insufficiency 390 

xi 


xii  CONTENTS. 

PAGE 

VII.    Tricuspid  Insufficiency 398 

VIII.    Tricuspid  Stenosis 406 

IX.    Pregnancy  and  Labor  in  Cases  of  Heart  Disease  413 

X.    Congenital  Heart  Dise.yse 421 

XI.    Heart-Block  and  Adams-Stokes  Syndrome 460 

XII.    Pericarditis 480 

XIII.  Wounds  of  the  Heart  and  Cardiac  Trauma 513 

XIV.  Aneurism 521 


PART  IV. 
FUNCTIONAL  DISEASES  WITHOUT  ANATOMICAL  LESION. 

I.    Paroxysmal  Tachycardia 560 

II.    Thyroid  Heart 574 

III.    Miscellaneous    Disturbances    of   Cardiac    Function  —  The    So-called 

"  Cardiac  Neuroses  "  and  "  Cardiac  Neurasthenia  " 593 


LIST   OF   ILLUSTRATIONS 


■FIG.  PAGE 

1.  The  heart  and  great  vessels,  viewed  from  the  front frontispiece 

2.  The  heart  and  great?  vessels,  from  behind frontispiece 

3.  Relations  of  the  heart  and  great  vessels,  viewed  from  the  front xxiv 

4.  The  heart  and  thoracic  viscera,  Aaewed  from  behind xxiv 

5.  Sagittal  section  of  the  thorax,  viewed  from  the  right xxiv 

6.  Heart  muscle-fibres 1 

7.  Section  through  the  endocardium,  showing  section  of  the  muscle-fibres 2 

8.  Apparatus  for  perfusing  the  mammalian  heart 3 

9.  The  auricular  end  of  the  human  heart,  viewed  from  the  right 5 

10.  The  sinus  region  of  the  heart,  the  veno-auricular  or  venosinal  bands  of  striated 

muscle,  and  the  auriculo(atrio)ventricular  or  sinoventricular  muscle  bundle. .  .  6 

11.  Arrangement  of  ventricular  muscle-fibres 8 

12.  Apparatus  for  registering  the  volume  of  the  ventricles 9 

13.  Volume  curves  of  the  ventricles  at  different  heart  rates 9 

14.  Methods  for  demonstrating  the  movements  of  the  heart  valves 10 

15.  Voliune  curves  showing  the  effect  of  variations  in  venous  pressure  and  in  tonicity 

upon  the  rate  at  which  the  ventricles  are  filled  during  diastole 12 

16.  Volume  curve  showing  the  effect  of  low  venous  pressure  or  of  high  tonicity  upon 

the  amount  of  blood  entering  the  ventricles 12 

17.  Diagram  illustrating  the  changes  in  volume  of  the  ventricles  in  systole  and  diastole 

associated  with  variations  in  tonicity  and  systolic  output 12 

18.  Origin  and  course  of  the  cardiac  nerves,  and  cutaneous  distribution  of  the  corre- 

sponding schematic  branches 14 

19.  Curve  of  intraventricular  and  aortic  pressures 18 

20.  Riva-Rocci  blood-pressure  apparatus  as  modified  by  Stanton 20 

21.  Correct  method  of  feeling  the  pulse  in  Strasburger's  determination  of  minimal 

pressure 21 

22.  Erlanger  blood-pressure  apparatus  with  Hirschfelder  polygraph  attachment ....  21 

23.  Diagram  showing  arrangement  of  Erlanger  apparatus 22 

24.  Curve  taken  with  the  Erlanger  apparatus,  showing  points  of  maximal  and  minimal 

pressures 22 

25.  V.  Recklinghausen  apparatus  for  determining  the  maximal  and  minimal  blood- 

pressure  in  man 22 

26.  Diagram  showing  the  maximal  and  minimal  pressures  in  various  parts  of  the 

circulatory  system 24 

27.  Diagram  showing  effects  of  vasoconstriction,  vasodilation,  increased  and  decreased 

force  of  ventricular  contraction  upon  the  maximal  and  minimal  blood-pressures 

and  upon  the  form  of  the  pulse 25 

28.  Mosso  plethysmograph 26 

29.  Diagram  showing  the  curve  of  blood-pressure  during  asphyxia 27 

30.  Diagram  showing  typical  blood-pressures  in  various  diseases 29 

31.  Hooker  and  Eyster's  modification  of  V.  Recklinghausen's  method  of  determining 

the  venous  pressure  in  man 33 

32.  Determann's  apparatus  for  determining  the  viscosity  of  the  blood 38 

33.  Brachial  pulse-curves  taken  with  the  Erlanger  blood-pressure  apparatus  from  the 

arms  of  two  patients 42 

xiii 


xiv  LIST  OF  ILLUSTRATIONS. 

34.  Absolute  sphygmograms,  all  of  which  correspond  to  the  radial  tracing  above 43 

35.  Significance  of  the  pulse-curve 44 

36.  Diagram  showing  the  time  relations  of  ventricular  volume  and  pressure  curves  to 

pulse  tracings  from  the  aorta,  carotid  and  radial  arteries 44 

37.  Three  types  of  arterial  pulse-curve  corresponding  to  the  same  pulse-pressure  and 

same  pulse-rate 45 

38.  Effect  of  inhalation  of  amyl  nitrite  upon  the  pulse  form 45 

39.  Mercury  manometer  tracing  from  the  carotid  artery  of  a  dog,  showing  rhythmic 

variations  in  blood-pressure  and  rhythmic  increase  in  dicrotism 46 

40.  Diagram  showing  various  forms  of  pulse-curve  encountered  clinically 46 

41.  Sites  for  recording  the  jugular  and  carotid  pulsations 51 

42.  Apparatus  for  recording  the  respiration 52 

43.  V.  Jaquet's  cardiosphygmograph 52 

44.  Normal  venous  tracings 53 

45.  Diagram  representing  the  various  events  in  a  cardiac  cycle 53 

46.  Venous  tracing  showing  absence  of  the  c  wave  in  a  case  of  heart  failure 54 

47.  Venous  tracing  showing  auricular  paralysis  (absence  of  a  wave)  with  large  (x) 

depression 54 

48.  Venous  tracing  from  a  very  slow  heart,  with  loud  third  heart  sound,  showing  the 

presence  of  the  h  wave 56 

49.  Tracing  from  the  same  person  one  hour  later,  after  giving  atropine  and  quickening 

the  pulse 56 

50.  Showing  a  wave  w  occurring  shortly  before  the  a  wave 56 

51.  Positive  or  ventricular  type  of  venous  pulse  in  tricuspid  insufficiency,  showing 

absence  of  the  a  wave 57 

52.  Positive  or  ventricular  type  of  venous  pulse  in  tricuspid  insufficiency,  showing 

absence  of  the  a  wave 57 

53.  Method  of  taking  tracing  from  the  oesophagus  to  show  the  contractions  of  the  left 

auricle 58 

54.  (Esophageal  and  carotid  tracings  from  a  normal  man 58 

55.  Simplest  form  of  apparatus  for  recording  the  electrocardiogram  and  cardiogram 

simultaneously 59 

56.  Patient  with  both  hands  in  salt-solution  jars  ready  for  taking  electrocardiogram . .  59 

57.  Course  of  the  electrical  variations  due  to  the  heart-beat  in  man 59 

58.  Normal  electrocardiogram  showing  the  time  relations  to  the  venous  and  carotid 

pulse-waves 59 

59.  Normal  electrocardiogram 59 

60.  Diagram  representing  various  types  of  irregular  pulse 63 

61.  Respiratory  arrhythmia 64 

62.  Venous  tracings  in  heart-block.     Partial  heart-block  (3  :  1  rhythm)  during  pres- 

sure on  the  vagus,  in  a  case  of  Adams-Stokes  disease 66 

63.  Venous  tracings  in  heart-block.     Complete  heart-block  in  a  case  of  Adams-Stokes 

disease 66 

64.  Occasional  absence  of  apex  impulse  during  inspiration  simulating  interventricular 

heart-block 67 

65.  Alternating  pulse  in  a  case  of  paroxysmal  tachycardia 68 

66.  Response  of  frog's  ventricle  to  abnormal  stimuli 68 

67.  Tracing  from  jugular  vein  and  brachial  artery  in  man,  showing  ventricular 

extrasystoles 69 

68.  Tracings  from  the  jugular  vein  and  brachial  artery  of  a  patient  with  trigeminal 

pulse 69 

69.  Diagrammatic  reproduction  of  the  electrocardiogram  obtained  in  the  dog  as  the 

result  of  extrasystoles 70 

70.  Electrocardiogram  of  a  patient  with  mitral  stenosis,  showing  extrasystoles 70 


LIST  OF  ILLUSTRATIONS.  xv 

71.  Volume  curve  of  the  ventricles,  showing  the  dilatation  which  followed  the  entrance 

of  an  air-bubble  into  the  right  auricle 71 

72.  Extrasystoles  with  shortened  conduction  time,  supposed  to  arise  in  the  auriculo- 

ventricular  bundle 73 

73.  Variations  in  conduction  time  in  a  case  of  mitral  stenosis 73 

74.  Tracing  showing  absolute  arrhythmia  with  weak  ineffectual  systoles 74 

75.  Diagram  showing  the  alterations  of  rhythm  which  may  cause  a  pulsus  bigeminus . .  74 

76.  Absolute  permanent  irregularity  with  a  wave    preserved  in  a  case  of  mitral 

stenosis 75 

77.  Perpetually  irregular  pulse  with  absence  of  a  wave 76 

78.  Electrocardiogram  from  a  case  of  perpetual  absolute  arrhythmia  showing  extra- 

systole  77 

79.  EfTect  of  arrhythmia  on  the  circulation,  blood-pressure,  and  volume  of  the 

ventricles 77 

80.  Radiograph  of  normal  chest 83 

81.  X-ray  shadows  in  different  axes  of  the  body 84 

82.  A  simple  form  of  orthodiagraph 85 

83.  Diagram  showing  the  use  of  the  orthodiagraph 85 

84.  Orthodiagraphic  outline  of  normal  heart,  showing  Moritz's  conjugates 85 

85.  Movements  of  the  heart  leading  to  the  protrusions  and  retraction  during  systole .  .  89 

86.  Rubber  funnel  for  cardiographic  tracings 90 

87.  Cardiograms  obtained  over  right  and  left  ventricles 90 

88.  Various  forms  of  apex  tracings 91 

89.  Areas  of  pulsation  and  retraction 92 

90.  Eddies  producing  thrills  as  illustrated  by  a  stream  of  water 92 

91.  Goldscheider's  orthopercussion 93 

92.  Percussion  with  the  orthoplessimeter 94 

93.  Diagram  to  show  the  cause  of  unavoidable  error  in  percussion  of  the  cardiac 

outlines 95 

94.  Areas  of  cardiac  dulness  and  flatness  in  a  normal  man 95 

95.  Cardiac  outlines  in  a  child  of  nine  years 96 

96.  Diagrams  illustrating  the  movements  of  the  normal  heart  on  change  of  posture 

from  side  to  side,  and  in  the  various  phases  of  respiration 97 

97.  Graphic  records  of  the  heart  sounds 98 

98.  Diagram  for  representing  the  heart  sounds  in  clinical  notes 99 

99.  Choice  of  stethoscope  bells 101 

100.  The  "valvular  areas " 102 

101.  The  propagation  of  the  heart  sounds  from  valves  to  chest  wall 103 

102.  Graphic  records  of  the  fetal  heart  sounds 104 

103.  Diagram  illustrating  the  split  sounds  and  gallop  rhythms  and  their  phonetic 

equivalents 105 

104.  Graphic  record  of  a  split  pulmonic  second  sound 106 

105.  Graphic  record  of  the  third  heart  sound 107 

106.  Jugular  and  carotid  tracings  from  a  normal  individual  with  a  well-marked  third 

heart  sound 108 

107.  Forces  supposed  to  be  at  work  in  the  production  of  the  third  heart  soimd 108 

108.  Similarity  between  the  production  of  voice  sounds  and  the  production  of  murmurs  110 

109.  Distribution  of  the  accidental  murmur 114 

110.  Graphic  record  of  an  accidental  murmur 115 

111.  Diagram  showing  the  relation  of  the  more  common  simple  murmurs  to  events  of 

the  cardiac  cycle 116 

112.  Cardiac  dulness  in  v.  Leyden's  case  upon  his  three  successive  admissions 125 

113.  Alterations  of  blood-pressure  due  to  rapid  lifting  of  light  weights  with  the  feet. .  130 

114.  Effect  on  patient  with  badly  broken  eompensation  of  walking  on  a  level 131 


xvi  LIST  OF  ILLUSTRATIONS. 

115.  Effect  of  prolonged  exercise  upon  the  blood-pressure  of  men  in  various  degrees  of 

muscular  strength 131 

116.  Rise  of  blood-pressure  during  Valsalva's  experiment  and  during  exercise 132 

117.  Variations  in  size  of  the  heart  of  a  long-distance  bicycle  rider,  as  the  result  of  a 

very  long  race 133 

118.  Effect  of  strain  upon  the  dog's  heart  whose  tonicity  is  good 135 

119.  Volume  curve  of  a  dog  whose  cardiac  tonicity  is  low 136 

120.  Effect  upon  the  volume  of  the  dog's  heart  produced  by  clamping  the  descending 

thoracic  aorta 137 

121.  Diagram  showing  changes  in  the  circulation:   I,  normal;   II,  broken  pulmonary 

compensation;    III,  broken  systemic  compensation;    IV,  both  compensations 
fail ;  stases  in  lungs  and  veins 139 

122.  The  two  types  of  Cheyne-Stokes  respiration  in  their  relations  to  the  blood-pressure 

curves 152 

123.  Legs  of  a  patient  with  extreme  oedema  and  tremendous  ulcers 154 

124.  Curschmann's  modification  of  the  Southey  tubes  for  draining  oedema  of  the  legs .  .  155 

125.  Electrical  record  of  afferent  impulses  travelling  up  the  vagi 157 

126.  Insertion  of  the  knife  in  venesection 166 

127.  Effect  of  venesection  on  the  cardiac  outline,  showing  diminution  in  size  of  right 

heart , 167 

128.  Typical  effect  of  venesection  upon  the  circulation 167 

129.  Tracing  showing  the  action  of  digitaUs  upon  the  dog's  blood-pressure 175 

130.  Variations  in  blood-pressure  in  a  patient  imder  the  influence  of  digitalis  and 

nitroglycerin 176 

131.  Effect  of  digitalis  on  cardiac  tonicity  in  the  dog 177 

132.  Curve  showing  the  effect  of  strychnine  upon  cardiac  tonicity 182 

133.  Effects  of  drugs  of  the  nitrite  series  upon  the  blood-pressure  in  man 187 

134.  Schott  resisted  movements 196 

135.  Orthodiagraphic  outline  of  a  patient  with  dilated  heart,  showing  the  effect  of 

Schott  movements 197 

136.  Hypertrophic,  normal,  and  atrophic  hearts 203 

137.  Photomicrographs  of  atrophic  and  hypertrophic  heart  muscle 204 

138.  Heart  of  normal  dog  and  of  dog  which  has  run  for  three  months  on  a  treadmill .  .   206 

139.  Areas  of  pulsation  and  retraction  hypertrophy  of  the  right  and  left  ventricles ....   209 

140.  Diagram  showing  power  of  normal  and  hypertrophied  (athlete's)  heart  at  rest  and 

during  exercise,  compared  with  that  of  a  diseased  heart 211 

141.  Distribution  of  fat  in  and  about  the  heart 214 

142.  Photomicrographs  of  fat  deposits  in  the  heart 215 

143.  An  excessive  deposit  of  epicardial  fat 216 

144.  Infiltration  along  the  course  of  the  blood-vessels  in  subacute  myocarditis;  blood- 

vessels injected 225 

145.  Septic  myocarditis  with  multiple  abscesses  in  the  heart  wall 226 

146.  Photomicrograph  showing  an  abscess  in  the  heart  muscle 227 

147.  Orthodiagraphic  outlines  of  the  heart  of  a  child  during  the  course  of  a  severe 

diphtheria 230 

148.  Specimen  showing  a  cardiac  aneurism  covered  with  pericardial  adhesions 234 

149.  Chronic  myocarditis  (cardiosclerosis) 234 

150.  Specimens  showing  chronic  myocarditis 235 

151.  Hypertrophy  of  some  muscle  bundles  in  the  auricle  with  atrophy  (transparency) 

of  other  areas 236 

152.  Curve  of  blood-pressure  in  a  case  of  chronic  myocarditis;  high  blood-pressure  per- 

sisting until  shortly  before  death 237 

153.  Various  types  of  arteriosclerotic  lesions.     (Schematic.) 251 

154.  Cross  section  of  a  radial  artery  showing  arteriosclerotic  changes  in  the  media ....   252 


LIST  OF  ILLUSTRATIONS.  xvii 

155.  Arteriosclerosis  of  the  descending  aorta,  showing  atheromatous  plaques 253 

156.  Atheromatous  plaque,  showing  the  changes  in  the  intima 254 

157.  Tortuous  radial  artery 260 

158.  Retinal  changes  in  arteriosclerosis 260 

159.  Effect  of  arteriosclerosis  upon  the  circulation 261 

160.  Blood-pressure  chart  of  case  of  typical  vasomotor  crises 271 

161.  Blood-pressure  chart  showing  a  vascular  crisis  of  the  cerebral  type 272 

162.  Diagram  to  illustrate  the  elimination  of  COj  by  the  blood  in  normal  and  sclerotic 

arteries 273 

163.  Thromboangitis  obliterans  and  endarteritis  obliterans 276 

164.  Hands  and  feet  of  a  patient  with  Raynaud's  disease,  showing  gangrenous  ulcers 

and  the  stumps  of  amputated  toes 277 

165.  Effect  of  ligation  of  a  large  coronary  artery  upon  the  blood-pressure 280 

166.  Sclerosis  of  a  coronary  artery,  producing  an  area  of  infarction  near  the  apex.  . .  .   282 

167.  Distribution  of  pain  in  attacks  of  angina  pectoris 286 

168.  Distribution  of  attacks  of  pain  and  sensory  disturbances  in  a  case  of  angina 

pectoris ,   287 

169.  Blood-pressure  curve  showing  crises  of  hypertension  during  attacks  of  angina 

pectoris 288 

170.  Fibrinous  deposit  upon  an  aortic  cusp  one  hour  after  mechanically  injuring  the 

valve 299 

171.  Mitral  endocarditis  showing  large  vegetations 300 

172.  Injection  of  chronically  inflamed  valves 300 

173.  Structure  of  the  normal  auriculoventricular  valve 301 

174.  Photomicrograph  of  a  specimen  showing  acute  and  subacute  endocarditic  lesions 

upon  the  mitral  valve 302 

175.  Portals  of  infection  in  endocarditis 303 

176.  Temperature  curve  from  a  case  of  malignant  endocarditis 305 

177.  Temperature  curve  from  a  case  of  simple  acute  endocarditis 305 

178.  Diagram  showing  relative  frequency  of  the  most  important  valvular  lesions  at 

various  ages 312 

179.  Diagram  showing  the  relative  frequency  of  the  various  valvular  lesions  in  cases  of 

valvular  heart  disease 312 

180.  Regurgitant  streams  in  organic  and  functional  mitral  insufficiencies 322 

181.  Diagram  showing  the  volume  and  pressure  curves  under  these  conditions 324 

182.  Curve  of  intraventricular  pressure  in  mitral  insufficiency  produced  on  a  mechanical 

model 325 

183.  Diagram  showing  the  effects  of  mitral  insufficiency  upon  the  circulation 326 

184.  Distribution  of  the  murmur  in  mitral  insufficiency 329 

185.  Cross  section  of  the  body  showing  how  the  murmur  reaches  the  chest  wall 330 

186.  Radiograph  of  a  patient  with  mitral  insufficiency,  showing  horizontal  enlarge- 

ment of  the  heart  to  the  left 330 

187.  Diagram  of  Fig.  186,  showing  the  directions  in  which  cardiac  enlargement  has 

taken  place 331 

188.  Graphic  records  of  the  heart  sounds,  showing  the  systolic  murmur 331 

189.  Human  heart,  showing  mitral  and  tricuspid  stenosis;  viewed  from  above;  the 

auricles  have  been  cut  through 341 

190.  Diagram  showing  the  changes  in  the  circulation  due  to  mitral  stenosis 343 

191.  Volume  of  the  ventricles  in  experimental  mitral  stenosis 344 

192.  The  variations  in  the  volume  curve  of  the  ventricles  in  increasing  degrees  of  mitral 

stenosis 344 

193.  Direction  of  the  stream  entering  the  left  ventricle  through  the  stenotic  mitral 

orifice 346 

194.  Cardiac  outline  and  distribution  of  the  presystolic  rumble  in  mitral  stenosis 347 

B 


xviii  LIST  OF  ILLUSTRATIONS. 

195.  Radiograph  from  a  case  of  mitral  stenosis,  showing  increase  of  the  shadow  due  to 

the  dilated  left  auricle 348 

196.  Diagram  representing  the  shadows  shown  in  Fig.  195 348 

197.  Graphic  record  of  carotid  pulse  and  heart  sounds  in  mitral  stenosis 348 

198.  Diagram  showing  the  relations  of  the  various  sounds  heard  in  uncomplicated 

mitral  stenosis  to  events  in  the  filling  and  emptying  of  the  ventricle 349 

199.  Venous  pulse  of  a  patient  with  mitral  stenosis  during  an  attack  of  acute  heart 

failure 350 

200.  Permanent  arrhythmia  in  a  case  of  mitral  stenosis,  showing  persistence  of  the 

auricular  contractions  (a  wave)  upon  the  venous  pulse 354 

201 .  Specimen  showing  vegetations  upon  the  aortic  valves 360 

202.  The  various  forms  of  lesion  producing  aortic  insufficiency 361 

203.  Effect  of  aortic  insufficiency  in  the  mechanical  model 362 

204.  Diagram  of  the  circulation  in  aortic  insufficiency 363 

205.  Diagram  showing  how  the  high  cardiac  tonicity  hastens  the  efjuilibrium  between 

aortic  pressure,  intraventricular  pressure,  and  tonicity,  and  thus  diminishes 
the  amount  of  blood  regurgitating 364 

206.  Effect  of  rupturing  an  aortic  valve  in  a  dog,  showing  a  transitory  dilatation 

followed  by  a  permanent  diminution  in  size 364 

207.  Area  of  cardiac  dulness  and  distribution  of  the  cardiac  sounds  and  murmurs  in 

aortic  insufficiency 368 

208.  Radiograph  of  a  case  of  aortic  insufficiency,  showing  elongation  of  the  long  axis  of 

the  heart 368 

209.  Diagram  of  Fig.  208,  showing  the  hypertrophy  of  the  left  ventricle 368 

210.  Direction  of  the  primary  regurgitant  streams  in  aortic  insufficiency 370 

211.  Relation  of  murmurs  in  aortic  insufficiency  to  the  cardiac  cycle 371 

212.  Functional  mitral  stenosis  in  aortic  insufficiency  as  demonstrated  on  the  excised 

heart  by  Baumgarten's  method 371 

213.  Variations  in  the  form  of  the  pulse-wave  encountered  clinically  in  aortic  insuffi- 

ciency    372 

214.  Tracings  from  a  dog  with  experimental  aortic  insufficiency,  showing  the  con- 

version of  a  collapsing  into  an  anacrotic  pulse  by  clamping  the  descending  aorta  373 

215.  Radial  pulse  tracings  showing  extrasystoles,  probably  of  ventricular  origin 374 

216.  Specimen  showing  aortic  stenosis.     Viewed  from  above 381 

217.  Forms  of  stenotic  aortic  orifices 381 

218.  Carotid  pulse  and  intraventricular  pressure  in  experimental  aortic  stenosis 382 

219.  Diagram  of  the  circulation  showing  the  effect  of  aortic  stenosis 38.3 

220.  Diagram  showing  the  cardiac  outline  and  distribution  of  the  murmur  in  aortic 

stenosis 384 

221.  Murmur  of  aortic  stenosis 385- 

222.  Diagram  showing  the  pulsus  tardus  and  the  anacrotic  type 38& 

223.  Pulse  tracings  from  cases  of  aortic  stenosis 386- 

224.  Diagram  of  the  circulation  in  pulmonary  insufficiency 391 

225.  Distribution  of  the  murmur  in  pulmonary  insufficiency 392 

226.  The  outline  of  a  normal  heart  superposed  upon  that  of  a  dilated  heart,  showing  the 

enlargement  of  the  tricuspid  orifice 397 

227.  Diagram  showing  the  changes  in  the  circulation  in  tricuspid  insufficiency 398 

228.  Venous  pulse  of  patients  with  tricuspid  insufficiency  (positive  venous  pulse) 399 

229.  Venous  pulse  of  another  patient 399' 

230.  Distribution  of  the  murmur  and  cardiac  outline  in  tricusj)id  insufficiency 401 

231.  Cross  section  of  the  body,  showing  the  paths  of  propagation  of  the  murmur  of 

tricuspid  insufficiency 401 

232.  Tracings  of  liver  pulsation 402 

233.  Systolic  pulsation  of  the  liver  of  patient  W.  H 403. 


LIST  OF  ILLUSTRATIONS.  xix 

234.  Diagram  showing  the  changes  in  the  circulation  in  tricuspid  stenosis 408 

235.  Cardiac  outline  and  distribution  of  the  presystolic  rumble  and  snapping  first 

sound  in  tricuspid  stenosis 409 

236.  Very  early  stage  in  the  development  of  the  human  circulatory  system 421 

237.  Human  embryo  4  mm.  long 422 

238.  Heart  of  an  embryo  4  mm.  long  slightly  older  than  that  shown  in  Fig.  237,  show- 

ing the  earliest  stages  in  the  formation  of  two  auricular  and  two  ventricular 
pouches 423 

239.  A  diagram  showing  the  interior  of  this  heart 423 

240.  Development  of  the  arterial  system  from  out  of  the  primitive  aortic  arches 423 

241.  Heart  of  slightly  older  embryo,  showing  separation   of  aortic  and  pulmonary 

channels  in  truncus  arteriosus 424 

242.  Still  later  stage,  showing  the  complete  division  of  the  truncus  arteriosus  into 

pulmonary  artery  and  aorta » 425 

243.  Auricular  end  of  the  same  heart 425 

244.  Development  of  the  pericardial  cavity 426 

245.  The  circulation  in  the  foetus  just  before  birth 428 

246.  Pulmonary  stenosis  due  to  fusion  of  the  cusps 431 

247.  Pulmonary  stenosis  due  to  a  lesion  of  the  infundibulum 431 

248.  Complete  pulmonary  atresia 431 

249.  Schema  illustrating  the  genesis  of  pulmonary  stenosis 432 

250.  Currents  and  lines  of  force  in  the  embryonic  heart  which  result  from  pulmonary 

stenosis    and    tend    to    produce    patency    of   the    septa    and    of  the  ductus 
arteriosus 434 

251.  Three-chambered    heart    (cor   biatriatum    triloculare)    produced    by    complete 

atresia  of  the  pulmonary  and  tricuspid  orifices 435 

252.  Diagram  of  the  circulation  in  pulmonary  stenosis  and  atresia 436 

253.  Dilatation  and  irregularity  of  the  retinal  vessels 439 

254.  Clubbed  fingers 439 

255.  Distribution  of  the  pulmonary  systolic  murmur  of  pulmonary  stenosis 440 

256.  Direction  of  blood-streams  and  propagation  of  murmurs  accompanying  defect  in 

the  interventricular  septum,  pulmonary  stenosis,  and  open  ductus  arteriosus .  .  440 

257.  Distribution  and  character  of  the  murmur  due  to  a  patent  interventricular 

septum  (Roger's  murmur) 444 

258.  Open  foramen  ovale 446 

259.  Diagram  showing  a  cross  section  of  the  same 446 

260.  Openings  between  strands  of  muscle  in  the  interauricular  septum 447 

261.  Radiograph  of  a  thirteen  year  old  boy  with  patent  ductus  arteriosus  and  aneuris- 

mal  dilatation  of  the  ductus  and  pulmonary  artery 451 

262.  Stenosis  of  the  isthmus  of  the  aorta  above  the  ductus  arteriosus,  type  of  the 

new-born 453 

263.  Stenosis  below  the  ductus  arteriosus,  adult  type 454 

264.  Transposition  of  the  viscera  in  embryo  and  adult 456 

265.  Transposition  of  the  valves 457 

266.  Pulmonary  artery  with  four  cusps 457 

267.  Tracing  of  the  apex  beat  in  a  case  of  Adams-Stokes  disease 461 

268.  Partial  heart-block  (3  :  1  rhythm)  produced  by  pressure  upon  the  vagus  in  a 

patient  with  disturbed  conductivity  who  was  also  subject  to  attacks  of  the 
Adams-Stokes  syndrome 462 

269.  The  right  branch  of  the  auriculoventricular  bundle  in  the  dog's  heart 463 

270.  Tracings  from  the  carotid  artery  and  the  jugular  vein  of  a  patient  with  Adams- 

Stokes  disease 464 

271.  The  Erlanger  heart-block  clamp  compressing  the  auriculoventricular  bundle 465 

272.  Effect  of  gradually  tightening  the  clamp 465 


XX  LIST  OF  ILLUSTRATIONS. 

273.  Tracing  from  jugular  vein  and  carotid  artery  in  a  case  of  complete  heart-block 

after  the  syncopal  attacks  had  subsided 467 

274.  Diagram  representing  the  conditions  found  in  the  tracing  Fig.  273 468 

275.  Heart  of  a  patient  showing  calcifications  which  produced  Adams-Stokes  disease . .  469 

276.  Diagram  showing  the  two  types  of  ventricular  stoppage  producing  the  Adams- 

Stokes  syndrome 470 

277.  Section  of  a  luetic  infiltration  of  the  auriculoventricular  bundle 470 

278.  Acute  fibrinous  pericarditis 482 

279.  Tuberculous  pericarditis  (cor  villosum) 482 

280.  Diagram  showing  the  relations  of  the  pericardial  and  pleural  frictions  to  the 

cardiac  and  respiratory  movements 484 

281.  The  circulation  in  cases  with  pericardial  effusion 488 

282.  Area  of  cardiac  dulness  from  pericardial  effusion 489 

283.  Positions  of  the  heart  in  pericarditis  with  effusion 491 

284.  Radiograph  of  a  patient  with  pericardial  effusion 492 

285.  Sites  for  paracentesis  pericardii  and  pericardiotomy 496 

286.  Specimen  showing  the  two  layers  of  pericardium  united  in  some  parts  by  long 

strands  and  in  others  by  short  bands  of  dense  adhesions 500 

287.  Sections  showing  adherent  pericardium 501 

288.  Anterior  and  posterior  pericardial  adhesions.     (Semi-schematic) 502 

289.  Cardiac  outline  in  adherent  pericardium 505 

290.  Adhesions  causing  inspiratory  and  expiratory  dropping  of  beats  (Riegel's  pulse 

and  the  pulsus  paradoxus) 506 

291.  Radiograph  of  a  case  of  adherent  pericardium 507 

292.  Case  of  pericarditic  pseudocirrhosis 509 

293.  Wounds  of  the  left  ventricle 514 

294.  Exposure  of  the  heart  for  suturing  a  wound 516 

295.  Specimen  of  a  large  aneurism 521 

296.  Aneurism  arising  just  above  a  sinus  of  Valsalva 524 

297.  Aneurism  of  the  ascending  arch  and  innominate  artery 524 

298.  Aneurism  of  the  transverse  portion  of  the  aortic  arch  penetrating  through  the 

sternum 524 

299.  Aneurism  of  the  descending  aorta  eroding  the  vertebrae 524 

300.  Sections  through  the  wall  of  an  aneurism 525 

301.  Composite  figure  showing  the  relations  of  various  aneurisms  to  surrounding 

structures 528 

302.  Tracings  of  the  outlines  of  an  aneurism  of  the  innominate  artery,  showing  its 

growth  and  the  formation  of  secondary  prominences  upon  its  surface 529 

303.  Method  of  inspecting  for  pulsations 532 

304.  Effect  upon  the  circulation  of  interposing  an  inelastic  and  an  elastic  bulb  along 

the  course  of  an  artery  in  a  model  of  the  circulation 634 

305.  Effect  of  aneurisms  at  various  sites  upon  the  blood-pressure,  rate  of  transmission, 

and  the  form  of  the  pulse- wave 535 

306.  Radial  pulse  tracings  from  the  right  and  left  radial  arteries  of  a  patient  with 

aneurism  of  the  first  part  of  the  arch  of  the  aorta 535 

307.  Radiograph  of  a  patient  with  a  large  aneurism  of  the  ascending  aorta  and  the 

arch,  viewed  from  behind 536 

308.  Radiograph  of  a  patient  with  diffuse  dilatation  of  the  arch  of  the  aorta 537 

309.  Diagram  of  the  radiograph  shown  in  Fig.  308 537 

310.  Cardiac  dulness  in  cases  of  aneurism 540 

311.  Area  of  cardiac  dulness  in  a  patient  with  dilated  arch  of  the  aorta 543 

312.  Tumor  and  pulsation  in  a  case  of  aneurism  of  the  abdominal  aorta 545 

313.  Tortuous  subclavian  artery,  simulating  a  small  aneurism 546 

314.  Dissecting  aneurisms 547 


LIST  OF  ILLUSTRATIONS.  xxL 

315.  Diagram  showing  the  various  methods  for  the  operative  treatment  of  aneurism .  .   55S 

316.  Specimen  of  wired  abdominal  aneurism,  showing  an  island  of  clot  within  the  coils 

of  wire  surrounded  by  a  free  blood  channel 554 

317.  Venous  pulse  in  a  case  of  paroxysmal  tachycardia 561 

318.  Diagram  showing  the  various  types  of  tachycardia 562 

319.  Experimental  paroxysm  of  tachycardia  produced  by  faradization  of  the  dog's 

auricle 563 

320.  Diagram  showing  the  effect  of  a  paroxysm  of  tachycardia  upon  the  circulation ....   565 

321.  Photograph  of  a  patient  with  Basedow's  disease 579 

322.  Photograph  of  a  portion  of  the  thyroid  gland  removed  from  the  patient  shown 

in  Fig.  321 577 

323.  Drawing  of  a  histological  specimen  from  the  same  thyroid 57g 

324.  Diagram  showing  the  relation  of  the  various  anatomical  structures  concerned  in 

the  production  of  the  ocular  and  cardiac  manifestations  of  Basedow's  disease . .   584 

325.  Respiratory  arrhythmia  in  a  young  cigarette  smoker 594 

326.  Cross  section  of  the  thorax  of  a  flat-chested  individual,  showing  the  systolic 

heaving  of  the  chest  wall  and  the  forces  bringing  it  about 596 

327.  Low,  normal,  and  high  hearts.     (Semi-schematic.) 598 

328.  Radiograph  of  a  patient  with  dropping  heart  (bathycardia) 599 

329.  Photograph  of  a  patient  with  enteroptosis 6C2 


SYNONYMOUS  ANATOMICAL  TERMS. 


Old  Terminology. 

Basle  Anatomical  Nomenclature 

(BNA)  '. 

I.Atin. 

Auriculoventricular  groove . .  . 
Interventricular  septum 

Coronary  sulcus 

Sulcus  coronarius. 

Septum  of  ventricles 

Septum  ventriculorum. 

Muscular  septum  

Septum  musculare. 
Septum  membranaceum. 
Atrium. 

Membranous  septum 

Auricle 

Forechamber 

Auricular  appendix  

Auricle 

Auricula 

Int«rauricular  septum 

Columnae  carneae 

Septum  of  atria 

Septum  atriorum. 
Trabeculae  carneae. 

Fleshy  cords 

Annulus  ovalis 

Edge  of  oval  fossa 

Limbus  fossae  ovalis  (Vieus- 
senii) . 

Intervenous  tubercle  of  Lower 

Tuberculum  intervenosum 

(Loweri) . 

Eustachian  valve 

Valve  of  inferior  vena  cava.  . 

Valvula  venae  cavae   (infe- 
rioris,  Eustachii). 

Valve  of  Thebesius ;  coronary 
valve 

Value  of  coronary  sinus 

Valvula  sinus  coronarii  (The- 
besii) . 

Foramina  Thebesii 

Foramina  of  the  smallest 
veins 

Foramina  venarum  minim- 

arum  (Thebesii). 

Tricuspid  valve    (right  auri- 
culoventricular valve) 

Tricuspid  valve 

Valvula  tricuspidalis. 

Infundibular  cusp 

Anterior  cusp 

Cuspis  anterior. 

Cuspis  posterior. 

Cuspis  medialis. 

Valvula   bicuspidalis   (mi- 
tralis). 

Marginal  cusp 

Posterior  cusp 

Medial  cusp 

Bicuspid  or  mitral  valve  .... 

Septal  cusp 

Left  auriculoventricular  valve 

Corpora  Arantii 

Nodules  of  the  semilunar 
valves 

Noduli  valvulanim   semilu- 

narium. 

Ductus  arteriosus  (Botalli)   .  . 

Arterial  duct               .... 

Ductus  arteriosus  (Botalli). 

Fasciculus    atriovent  ricii- 
laris. 

Auriculoventricular    bundle 
(Kent,  His) 

Atrioventricular  bundle  (His) 

'  Quoted  from  Barker,  L.  F.,  Anatomical  Terminology,  with  special  reference  to  the 
BNA,  Phila.,  1907. 

The  Basle  Anatomical  Nomenclature  (BNA)  is  the  terminology  adopted  by  an  inter- 
national convention  of  anatomists  at  Basle  in  1895,  for  the  purpose  of  securing  uniformity 
of  terminology.  As  it  has  not  yet  supplanted  the  old  terminology  in  clinical  usage, 
the  latter  is  adhered  to  in  this  book,  though  the  BNA  terms  are  frequently  given  in 
parentheses. 


Fio.  3. — Relations  of  the  heart  and  great  vessels,  \'iewed  from  the  front.  SVC,  superior  vena 
cava;  R  A,  right  auricle  (atrium);  L  V,  left  ventricle;  R  V,  right  ventricle;  P  A,  pulmonary  artery; 
PL,  pleura. 


Fio.  4. — ^The  heart  and  thoracic  viscera  viewed 
from  behind.  The  lungs  have  been  cut  away.  L  A, 
left  auricle ;  L  V,  left  ventricle. 


Fia.  5. — Sagittal  section  of  the  thorax  viewed 
from  the  right.  AZ.,  great  azygos  vein ;  POST. 
MEDIAST.,  posterior  mediastinum';  ANTER. 
MEDIAST.,  anterior  mediastinum;  R  A,  right 
auricle  ;  PHREN,  right  phrenic  nerve. 


DISEASES 

OF  THE 

HEART  AND  AORTA 


PART   I. 

GENERAL  CONSIDERATIONS  AND  METHODS  OF  DIAGNOSIS. 


I. 
PHYSIOLOGICAL  CONSIDERATIONS. 

PROPERTIES    OF    HEART    MUSCLE. 

The  heart  is  composed  of  striated  muscle-fibres  which  differ  anatomi- 
cally from  the  skeletal  muscles  in  being  almost  devoid  of  connective-tissue 
sheaths  and  from  most  of  the  skeletal  muscles  ^  in  the  fact  that  they  anas- 
tomose freely  with  one  another,  forming  a  continuous  meshwork  of  muscle 


Fig.  6. — Heart  muscle-fibres,  X375.     (After  Piersol.) 

tissue  (Figs.  6  and  7).  Physiologically  heart  muscle  differs  from  skeletal 
muscle,  for  (1)  it  is  continually  undergoing  rhythmic  contractions,  and 
(2),  as  Bowditch  has  shown,  every  contraction  is  maximal. 

A  great  deal  of  perspicuity  has  been  added,  especially  to  the  clinical 
study  of  the  cardiac  function,  by  discriminating  between  influences  which 
affect  the  cardinal  properties  of  the  cardiac  muscle  (Engelmann).  One 
recognizes  those  which  affect   (1)    rhythmicity    (chronotropic   in- 

*  The  tongue  of  the  frog  and  some  other  forms  of  muscle  somewhat  resemble  heart 
muscle  in  structure. 

1 


DISEASES  OF  THE  HEART  AND  AORTA. 


fluences);  (2)  irritability  (bathmotropic);  (3)  conductivity 
(dromotropic)  ;  (4)  contractility  (inotropic),  as  well  as  (5) 
tonicity  (Mackenzie). 

Influences   improving  these   properties    are    designated    as    positive, 
those  which  depress  them  as  negative. 

Endothelium 


Subendotbelial  — jy&p-' 
stratum  ^" 


Heart  muscle 

Blood-vessel 
Fio.  7. — Section  through  the  endocardium  showing  cross-section  of  the  muscle-fibres.     (After  Piersol.) 


ORIGIN    OF   THE    HEART-BEAT. 

Role  of  the  Salts. — Merunowicz,  under  Ludwig's  direction,  demon- 
strated that  the  rhythmicity  of  the  heart  depended  not  only  upon  its 
intrinsic  characteristics  but  particularly  upon  the  action  of  the  inorganic 
salts  present  in  the  blood  serum.  Ringer  (1882),  and  later  Howell,  showed 
that  the  antagonistic  actions  of  potassium  and  calcium  salts  were  the 
factors  chiefly  concerned  in  determining  the  rhythm  of  the  heart,  while 
Loeb  and  his  pupil,  Lingle,  showed  that  \\dthout  the  sodium  salts  it 
would  not  beat  at  all.  Accordingly,  as  Loeb  and  Howell  agree,  the  heart- 
beat can  be  maintained  only  when  these  three  salts  or  their  ions  are 
present  in  certain  definite  proportions,  or  in  what  Loeb  has  termed  * '  a 
balanced  solution."  However,  while  Ringer  and  Howell 
believe  that  the  calcium  liberates  the  motive  power  of 
the  cardiac  contraction,  Loeb  and  his  pupils  believe 
that  this  is  done  by  the  sodium  and  that  the  calcium  and 
potassium  merely  keep  the  sodium  from  liberating  too  much. 

Their  mode  of  action  has  been  explained  by  Loeb  in  1899  in  the 
following  words: 

"  The  salts  or  electrolytes  in  general  do  not  exist  in  living  tissues  as  such  exchisively, 
but  are  partly  in  combination  with  proteids  (or  fatty  acids).  The  salts  or  electrolytes  do 
not  enter  into  this  combination  as  a  whole,  but  through  their  ions.  The  great  impor- 
tance of  these  ion-proteid  combinations  (or  soaps)  lies  in  the  fact  that  by  substitution  of 
one  ion  for  another,  the  physical  properties  of  the  proteid  change  (e.g.,  their  surface  ten- 
sion, their  power  to  absorb  water  or  their  viscosity  or  state  of  matter).  We  thus  possess 
in  these  ion-proteid  or  soap  compounds  essential  constituents  of  living  matter,  which  can 
be  modified  at  desire,  and  hence  enable  us  to  vary  and  control  the  life  phenomena  themselves. 
"Life  phenomena,  and  especially  irritability,  depend  upon 
the  presence  in  the  tissues  of  a  number  of  the  various  metal  pro- 
teids, or  soaps  (Na,  Ca,  K,  and  Mg)  in  definite  proportions. 
Solutions  of  Na-salts  produce  rhythmical  contractions  only  if  the  muscle  cells  contain 


PHYSIOLOGICAL  CONSIDERATIONS. 


Ca-ions  in  sufficient  numbers.  As  soon  as  there  is  a  lack  of  Ca-ions  in  the  tissues  the  Na- 
ions  are  no  longer  able  to  cause  rhythmical  contractions.  On  the  other  hand,  if  we  add 
Ca-salts  in  sufficient  quantity  to  the  NaCl  solution,  it  will  no  longer  cause  rhythmical  con- 
tractions in  the  fresh  muscle  of  the  frog.  .  .  .  It  is  hardly  necessary  to  mention  that 
this  suggested  the  possibility  that  muscular  contraction  in  general  is  due  to  a  substitution 
of  Na  for  Ca,  or  vice  versa,  in  certain  compounds  (proteins  or  soaps)  in  the  muscle." 

The  hypothesis  that  the  main  physiological  antagonism  lies  between 
K  and  Ca  is  stated  by  Howell  in  the  following  words: 

"  The  well-nourished  heart  contains  a  large  supply  of  energy-yielding  material  which 
is  in  a  stable  form,  so  that  it  neither  dissociates  spontaneously  nor  can  be  made  to  do  so 
by  the  action  of  external  stimuli.  It  is  possible  that  this  stable,  non-dissociable  form  con- 
sists of  a  combination  between  it  and  the  potassium  or  the  potassium  salts,  and  that- 
therein  lies  the  functional  importance  of  the  potassium  contained  in  the  tissue.  This 
compound  reacts  with  the  calcium  or  with  the  calcium  and  sodium  salts  and  a  portion  of 
the  potassium  is  replaced;  and  a  compound  is  formed  which  is  unstable.  At  the  end  of 
the  diastolic  period  this  compound  reaches  a  condition  of  instability  such  that  it  disso- 
ciates spontaneously,  giving  rise  to  the  chain  of  events  that  culminates  in  the  normal 
systole.  Before  spontaneous  dissociation  occurs  it  may  be  hastened  by  an  external  stimu- 
lus, as  we  know  is  the  case  when  a  mechanical  or  electrical  shock  is  applied  to  the  heart  at 
any  time  after  diastole  begins." 

Any  single  ion  or  salt  is  poisonous  by  itself,  but  in  the  presence  of 
certain  others  may  be  beneficial.  This  very  interesting  question  of  "bal- 
anced ion  solutions"  has  been  extensively  investigated  by  Loeb  and 
his  pupils,  not  only  upon  heart  but  upon  skeletal  muscle  and  upon  lower 
medusae,  molluscs,  and  fishes. 

Even  the  mammalian  heart  can  be  readily  revived  and 
kept  beating  outside  the  body  if  perfused  with  a  solution  containing  these 
substances  together  with  sodium  bicarbonate  (Howell)  and  saturated  with 
oxygen  (Locke's  solution, — NaCl  0.9  per  cent.  +  CaClj  0.024  per  cent.  -1- 
KCl  0.42  +  NaHCOg  0.01  to  0.03  + 
dextrose  0. 1  per  cent.) .  It  is  necessary 
to  maintain  the  blood-pressure  at  50- 
100  mm.  Hg,  and  also  the  tempera- 
ture 36°  to  37°.  Kuliabko  and  others 
have  revived  excised  human  hearts 
many  hours  after  death.  Fibrillary 
contractions  occasionally  set  in,  but 
may  be  stopped  by  perfusing  with 
KCl  1.0  per  cent,  for  a  few  minutes 
instead  of  Locke's  solution.  The 
heart  then  comes  to  a  stand-still 
and  resumes  beating  under  Locke's 
solution. 

The  study  of  the  excised  heart  has  been  very  useful  both  in  testing 
the  effect  of  drugs  and  in  simulating  conditions  of  disease;  but  the  condi- 
tions of  circulation  are  not  exactly  comparable  to  those  within  the  animal, 
and  the  results  should  always  be  carefully  checked  upon  the  intact  animal 
before  assuming  them  to  be  normal  or  drawing  any  conclusions  as  to 
pharmacological  action. 

Myogenic  and  Neurogenic  Theories. — Whether  the  salts  or  ions  which 
maintain  the  rhythmicity  of  the  heart-beat  do  so  by  acting  directly  upon 


Fig.  8. — Apparatus  for  perfusing  the  maiftma- 
lian  heart.  A,  auricle;  V,  ventricle;  TAMB., 
tambour;  TH.,  thermometer;  MAN.,  manometer; 
GASCH,  gas  check;    O2,  tank  of  oxygen. 


4  DISEASES  OF  THE  HEART  AND  AORTA. 

the  muscle  tissue  (myogenic),  or  whether  the  stimuli  are  first  generated 
in  nerve  tissue  (neurogenic)  and  then  transmitted  to  the  muscle,  is  a 
question  which  has  been  disputed  for  centuries.  And  though  the  pendulum 
has  repeatedly  swung  from  one  opinion  to  the  other,  this  question  cannot 
at  present  be  answered.  It  is  quite  certain  that  all  the  extrinsic  cardiac 
nerves  can  be  removed  without  stopping  the  rhythmic  contractions,  and 
that  the  ganglion  cells  may  be  stimulated  without  materially  affecting  the 
rhythm  (Gaskell).  But  the  meshwork  of  muscle-fibres  in  the  heart  is  so 
permeated  by  a  meshwork  of  fine  nerve-fibres  that  it  has  been  impossible 
to  determine  whether  the  impulse  arises  in  the  muscle-cells  or  in  the  nerve 
endings  upon  their  surfaces.  Wm.  His,  Jr.,  has  indeed  shown  that  the 
heart  of  the  chick  embryo  beats  before  nerve-fibres  have  entered  it  at  all, 
but  the  possibility  still  remains  that  after  once  entering  the  heart  the 
nerves  may  take  the  initiation  of  contraction  away  from  the  adult  heart- 
muscle.  Moreover,  the  recent  experiments  of  Carlson  and  of  Magnus  in 
allied  fields  give  considerable  evidence  that  such  may  be  the  case;  so  that, 
in  spite  of  its  importance  for  both  the  physiology  and  the  pathology  of  the 
heart,  neither  the  myogenic  nor  the  neurogenic  theory  of  the  heart-beat 
has  been  finally  proved. 

Maximal  Contractions  and  Irritability. — As  Bowditch  has  shown,  the 
heart  liberates  all  its  available  energy  at  each  contraction,  which  resembles 
in  this  way  the  explosion  of  gunpowder  or  the  liberation  of  a  spring  by  a 
trigger.  Like  the  power  of  the  spring,  the  strength  of  the  cardiac  contrac- 
tion depends  upon  the  energy  stored  up.  This  energy  seems  to  depend 
upon  the  regeneration  of  the  contractile  substance  mentioned  above  by 
Howell.  When  the  next  contraction,  normal  or  abnormal  (extr  asystole), 
occurs  soon  after  the  last  (early  in  diastole),  the  contraction  is  weaker  than 
the  preceding,  since  it  liberates  less  energy,  but  the  contractile  substance 
is  again  completely  destroyed  and  requires  another  pause  (compensatory 
pause,  see  page  69)  to  regenerate  it.  When  it  occurs  late,  the  contrac- 
tion is  of  almost  or  quite  original  strength,  and  the  stored-up  energy  is  again 
liberated  completely.  Moreover,  Erlanger  has  shown  that  the  irritability  of 
the  heart  inci*eases  progressively  as  diastole  is  prolonged  and  as  the  muscle 
becomes  overloaded  with  the  energy-producing  substance. 

ORIGIN    AND    COURSE    OF    THE    CARDIAC   IMPULSE. 

The  Sinus  as  "Pace-maker"  of  the  Heart. — In  the  frog,  where  the 
cardiac  impulse  travels  slowly,  it  is  very  easy  to  see  that  it  arises  at  the 
sinus  venosus,  which  executes  a  contraction.  This  is  followed  by  contrac- 
tion of  the  auricle,  the  latter  after  an  appreciable  interval  by  a  visible  con- 
traction of  the  small  ring  of  muscle  about  the  auriculoventricular  ring 
(Bond),  and  this  in  turn  by  contraction  of  the  ventricles. 

It  is  probable  that  the  sinus  initiates  the  cardiac  rh3^thm,  because  it 
is  the  chamber  which,  when  isolated,  beats  at  the  fastest  rhythm  in  the 
blood-serum,  and  hence  it  becomes  what  Erlanger  terms  "the  pace-maker 
of  the  heart."  ^    Indeed,  if  the  impulse  from  the  sinus  is  blocked  by  crushing 

'  Under  pathological  conditions  and  especially  in  the  excised  heart  the  ventricle  may 
become  more  irritable  and  may  become  the  pace-maker  (reversed  rhythm). 


PHYSIOLOGICAL  CONSIDERATIONS. 


or  by  cooling  the  sino-auricular  border,  the  impulses  no  longer  reach  the 
auricles,  which  must  then  contract  by  their  own  slower  rhythm  or  not  beat 
at  all  (sinu-auricular  heart-block). 

Anatomy  of  the  Sinus  Region  in  Mammals.— In  man  and  other  mam- 
mals the  sinus  no  longer  exists  as  a  separate  chamber,  though  in  the  early 
embryo  (Fig.  243,  page  425)  its  homologue,  the  sinus  reuniens,  is  separated 
off  from  the  rest  of  the  auricular  cavity  by  the  Eustachian  valve.  This 
sinus  chamber  receives  the  two  vensB  cavae  and  the  coronary  sinus.  In 
the  course  of  development  the  growth  of  the  sinus  region  does  not  keep 
pace  with  that  of  the  auricle,  and  it  becomes  swallowed  up  in  the  latter, 
so  that  in  the  adult  the  sinus  corresponds  roughly 
to  the  area  bounded  by  the  mouths  of  the  two  venae 
cavae,  the  coronary  sinus,  and  the  interauricular 
septum. 


Systemic  aorta 
Pulmonary  aorta  or  artery 


Right  auricular  appendage 


it  ventricle,  conus 
arteriosus 


Sup.  pulm. 
vein 


Inf.  pulm. 
vein 

Fos8aovalis 
surrounded 
by  annulus 
Inferior 
vena  cava 


Orifice  of  coronary  ti;iu.~,  guaickd  by  Thebesian  valve 
Eustachian  valve  Depression  receiving  Thebesian  veins 

Fig.  9. — The  auricular  end  of  the  human  heart  viewed  from  the  right.     (After  Piersol.) 

Comparatively  little  is  known  concerning  the  structure  of  this  impor- 
tant region.  The  most  careful  studies  (Keith,  Retzer,  Schonberg)  are  con- 
cerned more  with  the  structure  of  the  veno-auricular  junction  or  the  sino- 
ventricular  connections  than  with  the  structure  of  the  sinus  as  a  whole, 
or  the  sinu-auricular  border  which  is  included  within  the  body  of  the 
right  auricle. 

The  Veno=auricular  Junction. — Schonberg  studied  the  veno-auricular  junction  in  a 
large  number  of  normal  and  abnormal  human  hearts  by  means  of  serial  sections,  each  series 
being  composed  of  300  to  800  sections.  At  a  level  10  to  15  mm.  above  the  entrance  of  the 
superior  vena  cava  into  the  auricle  (atrium)  he  found  the  usual  structure  of  vein  wall. 
Below  this  level  the  media  is  found  to  contain  groups  of  striated  muscle-fibres  separated 
from  one  another  by  fat  and  connective  tissue.    These  striated  muscle-fibres  arise  in  the 


6  DISEASES  OF  THE  HEART  AND  AORTA. 

vicinity  of  non-striated  fibres  but  are  never  continuous  with  them.  Bundles  of  these 
fibres  i  to  1  mm.  in  diameter  run  transversely  across  the  vein  toward  the  auricle,  gradually 
converging  into  larger  bundles,  which  are  separated  from  one  another  by  a  tissue  rich  in 
lymph-  and  blood-vessels.  In  the  angle  (sulcus)  formed  between  the  auricle  (atrium)  and 
vena  cava  these  bands  of  striated  muscle  become  much  thinner  and  contain  numerous 
tortuous  fibres  resembling  Purkinje  fibres.  In  this  region  there  is  a  considerable  deposit  of 
fat,  lymphoid  and  connective  tissue,  forming  a  more  or  less  definite  border-line.  The 
muscle-fibres  of  the  auricle  (atrium)  are  inserted  in  the  connective  tissue  here.  The 
connection  between  the  musculature  of  the  vena  cava  and  that 
of  the  auricle  is  made  by  the  numerous  small  bundles  of  striated 
muscle-fibres  lying  just  beneath  the  endocardium,  which  pa.ss  across  this  junc- 
tion and  end  in  the  fibres  of  auricular  muscle.  "In  the  macroscopic  prepa- 
rations it  is  almost  always  readily  seen  that  the  sulcus  is 
bridged  at  its  posterior  lateral  third  by  a  muscle-bundle  which 
ascends  upwards  and  backwards  from  the  auricle  (atrium)  to  the 
superior  vena   cava,  where  it  is   strengthened  by  fibres  from    the 


Fig.  10. — The  sinus  region  of  the  heart,  the  veno-auricular  or  veno-sinal  bands  of  -striated  musc'.e 
and  the  auriculo(atrio)ventricular  or  sinu-ventricular  muscle  bundle.  (Schematic,  constructed  from  the 
findings  of  Keith,  Schonberg,  and  Retzer.)  A.  Seen  from  the  right  side.  The  dotted  area  represents 
the  sinus  region ;  the  strije  represent  the  veno-auricular  muscle  strands.  V.C.S.,  superior  vena  cava; 
V.C.I.,  inferior  vena  cava;  SC,  coronary  sinus;  AVB.,  auriculo(atrio)ventricular  muscle  bundle 
(His  bundle);  TRIG,  tricuspid  valve;  PAP,  papillary  muscle.  B.  The  same  region  seen  from  the  front. 
MIT,  mitral  valve;  A  O,   aorta. 


circular  musculature  of  the  lower  part  of  the  vein.  This  bundle 
is  also  well  seen  microscopically,  but  numerous  other  smaller  muscle  bundles  are  seen  as 
well.  It  corresponds  quite  well  with  that  described  by  Keith  and  Flack,  and  Wenckebach. 
Schonberg  found  that  the  region  of  the  sulcus  is  particularly  rich  in  nerve-fibres, 
ganglion  cells,  blood-vessels,  and  lymphoid  tissue,  and  is  therefore  particularly  liable  to 
pathological  infiltrations  and  cicatrizations. 

It  is  worthy  of  note  that  the  sulcus  noted  by  Schonberg  does  not  repre- 
sent the  sinu-auricular  junction  but  the  veno-sinal  junction.  The  strands 
of  striated  muscle  which  he  describes  are  derived  from  the  sinus.  The  sinu- 
auricular  (sinu-atrial)  junction  on  the  other  hand  is  actually  situated  within 
the  body  of  the  auricle  (atrium). 

Role  of  the  Sinus  in  Mammals. — There  is  a  considerable  amount  of 
physiological  as  well  as  anatomical  evidence  that  in  the  adult  mammal 
as  well  as  in  the  amphibian  this  is  the  region  in  which  the  cardiac 
impulse  arises. 


PHYSIOLOGICAL  CONSIDERATIONS.  7 

MacWilliam  in  1888  was  able  to  show  that  this  intervenous 
area  was  the  only  region  at  which  the  application  of  heat 
quickened  and  cold  slowed  the  heart  rate.  Adam  and  the  writer 
were  able  to  confirm  this  observation.  H.  E.  Hering  has  shown  that  this  area  is 
often  the  last  to  cease  contraction  in  dying  mammalian  and  human  hearts,  though  this  is 
not  always  the  case  (Hirschf elder  and  Eyster).  Langendorff  and  Lehmann  and  also  Leon 
Fredericq  showed  that  even  in  the  excised  heart  portions  of  the  auricles  cut  off  from  this 
area  ceased  to  beat  or  beat  at  a  slow  rhythm,  while  those  which  remained  attached  to  the 
sinus  region  beat  at  about  the  original  rate.  Erlanger  and  Blackmann  were  able  to  produce 
halving  of  the  heart  rate  (sinu-auricular  block  ?)  by  torsion  of  this  area  in  the  excised  heart, 
but  like  Hirschfelder  and  Eyster  were  unable  to  produce  it  by  clamping  experiments 
upon  the  heart  in  situ.  The  most  conclusive  experiments  are  those  of  Lohmann  who 
poisoned  the  cells  in  tliis  area  by  direct  application  of  cotton  soaked  in  formalin,  and 
found  that  the  heart  at  once  slowed,  auricles  no  longer  followed  ventricles,  and  the  auricles 
and  ventricles  beat  simultaneously  (nodal  rhythm,  see  page  76). 

Course  of  the  Impulse  after  Leaving  the  Sinus.  —  From  the  sinus 
region  the  cardiac  impulse  travels  to  the  walls  of  the  auricles  and  gives 
rise  to  the  auricular  contraction.  It  is  also  propagated  downward  toward 
the  ventricles,  which  it  reaches  about  one-fifth  of  a  second  later. 

It  is  a  mooted  point  at  present  whether  the  path  from  sinus  to  ventricle  is  through 
auricular  tissue  or  whether  there  is  a  direct  sino- ventricular  pathway,  as  believed  by 
Retzer,  who  thinks  that  the  auricle  is  off  on  a  side  path  and  contracts  first  merely 
because  it  is  nearer  to  the  sinus  than  is  the  ventricle.  .However,  Bond's  observations 
on  the  frog,  showing  that  the  auricle  contracts  a  considerable  time  before  the  mus- 
culature of  the  auriculoventricular  ring,  indicates  that  the  impulse  passes  from  the 
former  to  the  latter. 

Kent,  His,  Retzer,  Braeunig,  Keith,  and  Tawara  have  shown  that  the 
cardiac  impulse  is  propagated  from  auricles  to  ventricles  through  the  system 
of  Purkinje  fibres,  which  forms  a  k  whose  shaft  arises  in  the  right  auricle 
at  or  near  the  sinus,  runs  in  the  membranous  septum  (auriculoventricular 
bundle)  downward  to  the  muscle  septum,  where  it  divides  into  two  branches 
which  straddle  the  muscular  septum  and  then  pass  to  the  right  and  left 
ventricles.  Within  these  chambers  the  branches  divide  into  numerous 
ramifications  which  lie  just  beneath  the  endocardium  and  pass  downward 
as  a  meshwork  of  light-colored  translucent  strands  to  the  papillary  muscles 
and  walls  of  the  ventricles.  Occasionally  instead  of  following  the  walls 
they  cross  the  ventricular  cavity  to  the  papillary  muscle  as  isolated  strands 
(moderator  bands,  T.  W.  King,  Tawara).  In  this  bundle  also  the 
presence  of  numerous  nerve-fibres  (Tawara)  and  of  ganglion  cells  (Gordon 
Wilson)  renders  it  doubtful  whether  the  impulse  travels  through  nerve  or 
muscle.     The  slow  time  of  transmission  is  a  little  in  favor  of  the  latter, 

COORDINATION    OF    THE    CARDIAC    CHAMBERS. 

Under  all  circumstances  (except  those  mentioned  on  page  67)  the 
contractions  of  both  auricles  and  of  both  ventricles  are  absolutely  synchro- 
nous. Barker  and  Hirschfelder  have  shown  that  simultaneous  contractions 
of  the  two  ventricles  continue  after  the  branch  of  the  conduction  system 
to  one  (the  left  ventricle)  has  been  cut,  and  hence  the  coordination  does 
not  depend  upon  the  auriculoventricular  conduction  system  but  upon  the 
ventricular  musculature. 


8 


DISEASES  OF  THE  HEART  AND  AORTA. 


Anatomy  of  the  Ventricular  Muscle. — This  is  not  surprising,  since,  as 
Ludwig,  Krehl,  and  J.  B.  MacCallum  have  shown,  each  strand  of  muscle- 
fibres  passes  from  ventricle  to  ventricle.  These  muscle-fibres  are  arranged 
in  three  distinct  layers  so  placed  that  they  are  wound  up  like  a  scroll,  the 
most  superficial  layer  of  the  left  ventricle  penetrating  to  become  the  deepest 
layer  of  the  right  (Fig.  11,  I,  II,  III).  Besides  these  MacCallum  has  de- 
scribed a  fourth  band  of  muscle,  independent  of  the  latter,  which  sur- 
rounds both  the  aortic  and  mitral  orifices  in  a  single  ring  of  muscle  (mitro- 
aortic  ring),  across  which  a  septum  of  connective  tissue  separates  the 
aortic  orifice  from  the  mitral  ring  (Fig.  11,  V).  This  band  is  more  or  less 
homologous  to  the  bulbus  arteriosus  of  the  lower  vertebrates,  and  plays 
a  most  important  role  in  preventing  leaks  at  the  valvular  orifices. 


II 


Fig.  1 1  .^Arrangement  of  ventricular  muscle-fibres.  (After  MacCallum.)  I  and  II,  superficial 
fibres  of  the  left  ventricle  and  conus  arteriosus  ;  III,  deep  layers  of  the  left  ventricle  ;  IV,  rings  of  muscle 
about  the  aortic  and  mitral  orifices;  V,  diagram  representing  these  relations.  LAV,  mitral  orifice; 
RAV,  tricuspid  orifice;  PA,  pulmonary  artery;  AO,  aorta;  PAP,  papillary  muscle;  AVB,  auriculo- 
(atrio)ventricular  bundle;  AORTIC,  ring  of  muscle-fibres  surrounding  both  the  aortic  and  mitral  orifices 
(mitro-aortic  ring). 


EMPTYING    AND    FILLING   OF    THE    HEART,    AND    MOVEMENTS 
OF    THE    VALVES. 

The  Presphygmic  Period. — The  instant  before  the  beginning  of  ven- 
tricular systole  the  mitral  and  tricuspid  valves  are  open,  while  the  aortic 
and  pulmonic  valves  are  closed.  When  the  ventricular  contraction  begins, 
it  at  once  raises  the  pressure  within  the  ventricles  above  that  in  the  auricles, 
causing  the  mitral  and  tricuspid  valves  to  close  with  a  snap.  There  is  thus 
a  short  interval,  the  presphygmic  (.07-.09  sec),  at  the  very  beginning  of 
systole,  during  which  all  four  valves  are  closed  and  movement  of  blood 
ceases  in  all  four  chambers.  This  period  lasts  until  the  pressure  within 
the  ventricles  rises  above  the  arterial  pressures  (minimal  pressure),  after 
which  the  blood  is  driven  out  during  the  rest  of  systole. 


PHYSIOLOGICAL  CONSIDERATIONS. 


9 


CA£p 


Fig.  12. — Apparatus  for  roistering  the  volume  of 
the  ventricles.     CARDJOM.,  cardiometer. 


Method  of  Recording  the  Volume  Curve. — Yandell  Henderson  has  recorded  the 
emptying  and  filling  of  the  ventricles  by  means  of  a  specially  constructed  cardiac  plethys- 
mograph  or  cardiometer  like  that  of  Tigerstedt  and  Johannson.  Henderson's  cardiometer 
was  made  from  an  ordinary  rubber  ball,  out  of  which  a  large  window  was  cut  and  then 
closed  hermetically  by  cementing  on  a  cur- 
tain of  rubber  dam.  In  the  centre  of  the 
rubber  dam  a  hole  was  cut  just  large  enough 
for  it  to  fit  air-tight  in  the  auriculoventricular 
groove.  The  heart  was  then  pushed  in 
through  the  hole  until  the  dam  slipped  into 
the  groove.  The  changes  of  pressure  within 
the  air  space  surrounding  the  heart  were  com- 
municated to  a  recording  tambour  through 
a  glass  tube  cemented  in  the  opposite  surface 
of  the  ball  (Fig.  12).  Dr.  Cameron  and  the 
writer  have  found  it  most  convenient  to  have 

the  recording  tambour  inverted,  so  that  upstrokes  record  systole  and  down- 
strokes  diastole,  while  a  general  rise  in  the  curve  indicates 
diminution    in    volume,   and  a   general    fall    indicates    dilatation. 

Outflow  during  Systole. — By  this  means  Henderson  has  found  that 
during  systole  the  ventricles  do  not  empt}'  themselves  with  a  rush  at  the 
beginning  of  systole,  but  that  the  outflow  continues  quite  uniform  through- 
out at  least  nine-tenths  of  the  latter  period  (outlasting  the  rise  of  the  arterial 
pulse-wave)  and  begins  to  slow  only  toward  the  very  end  (slight  rounding 
of  the  crest  of  the  curve).  At  the  cessation  of  outflow  there  is  an  instant 
during  which  the  ventricular  pressure  is  falling,  in  which  no  inflow  takes 
place,  but  this  is  only  one  or  two  hundredths  of  a  second  and  is  difficult  to 
estimate  accurately.  This  instant  corresponds  to  the  dicrotic  notch  upon 
the  aortic  pulse-wave. 

Filling  of  the  Ventricles. — The  ventricles  then  begin  to  fill  at  a  rapid 
and  uniform  rate  until  they  arc  almost  completely  distended.  If  the 
pulse-rate  is  rapid,  the  next  systole  takes  place  before  the  filling  is  as  com- 
plete as  possible,  and  cutting  short  the  filling  diminishes  the  volume  of  the 
heart;  not  only  the  total  volume,  but  the  amount  of  blood  discharged  at 
each  systole  (Fig.  13). 


AORTA 


VOLUME 

OF  VENTRICLES 


SLOW        NOR  MAL 


Fig.  13. — Volume  curves  of  the  ventricles  at  different  heart  rates.  (Modified  from  Henderson.) 
The  dotted  line  shows  how  the  curve  of  the  typical  cycle  may  be  sup)erposed  upon  the  curve  corresponding 
to  a  different  rate.     A,  quota  of  blood  forced  in  by  auricular  systole. 

Diastole  and  Diastasis. — If,  on  the  other  hand,  the  heart  rate  is  slow 
(Fig.  13),  as  after  stimulation  of  the  vagus,  the  influx  begins  at  the  same 
rate  as  before  and  continues  uniformly  for  about  two-fifths  of  a  second 
(steep  ascent  of  the  curve)  until  the  ventricles  are  distended,  after  which 
scarcely  any  blood  flows  into  the  ventricles  no  matter  how  long  the  interval 


10 


DISEASES  OF  THE  HEART  AND  AORTA. 


to  the  next  beat.  The  diastolic  period  is  thus  divided  into  two  parts :  (1)  the 
phase  of  diastole  proper  during  which  filling  of  the  ventricles 
takes  place;  (2)  the  phase  of  diastasis  in  which  little  or  no  filling 
occurs.  The  slower  the  heart  the  greater  is  the  disatolic  filling  and  the 
longer  its  duration.  The  greatest  amount  of  output  in 
unit  time  occurs  at  a  rate  which  just  allows  the  phase 
of  diastolic  filling  to  be  complete  but  in  which  the  next 
beat  occurs  before  diastasis  sets  in.  Any  rate  above  or  below  this  brings 
about  some  slowing  of  the  circulation. 

Position  of  the  Valves  in  Diastole. — Baumgarten  (1843)  has  been  abh  to  demonstrate 
upon  the  excised  heart  that  the  cusps  of  the  mitral  and  tricuspid  valves  are  floated  together 
by  the  influx  of  blood  and  the  valves  close  spontaneously  when  the  inflow  ceases.  The 
writer  has  been  able  to  show  that  the  occurrence  of  diastasis  is  not  necessarily  caused  by 
the  valves  being  closed,  but  by  the  fact  that  the  heart  fills  for  a  time  before  the  walls  are 


Fig.   14. 


-Methods   for   demoastrating  the  movements   of   the  heart  valves. 
Baumgarten 's  method. 


A,  Gad's  method ;    B, 


put  upon  a  stretch,  and  then  the  passive  elasticity  of  the  walls  prevents  further  filling. 
If  the  venous  pressure  is  materially  increased,  further  increase  in  volume  then  takes 
place.  The  closure  of  the  valves  in  early  diastole  depends  chiefly 
upon   the  suddenness   both   of    the  filling  and   of    its   cessation. 

A  very  pretty  and  instructive  demonstration  of  the  opening  and  closing  of  the  heart 
valves  has  been  devised  by  J.  Gad  by  an  experiment  shown  in  Fig.  14,  A,  which  can  be  very 
nicely  performed  upon  a  sheep's  heart  as  bought  at  a  butcher's  shop. 

The  left  auricle  is  cut  away  and  the  bowl  of  a  large  thistle  tube  tied  in  the  place  by 
a  circular  ligature.  A  large  glass  tube  is  thrust  through  the  aorta  into  the  ventricle  and 
ligatured  in  place.  Both  the  thistle  tube  and  the  aortic  cannula  are  connected  with  fun- 
nels by  means  of  rubber  tubes,  and  the  chambers  of  the  heart  may  be  then  completely 
filled  with  water.  The  opening  and  closing  of  the  valves  may  be  brought  about  by  raising 
and  lowering  one  or  the  other  of  the  funnels,  and  may  be  watched  through  the  wall  of  the 
bulb.  Insufficiency  of  the  valve  may  be  produced  by  cutting  or  stretching  one  of  the 
chordse  tendinese,  but  after  the  experiment  has  been  repeated  a  few  times  upon  the  same 
heart  a  certain  amount  of  insufficiency  usually  sets  in  spontaneously.  The  sounds  pro- 
duced by  the  valves  and  blood  stream  independently  of  the  contraction  can  be  well  studied 
by  placing  the  stethoscope  upon  such  a  heart,  provided  all  the  air  has  been  removed  from 
the  cardiac  chambers.    In  a  similar  manner  the  phenomena  can  be  observed  in  the  right 


PHYSIOLOGICAL  CONSIDERATIONS.  11 

heart.  The  closure  of  the  aortic  or  pulmonic  valves  can  also  be  demonstrated  by  drawing 
the  glass  tube  out  of  the  ventricle  up  into  the  vessel,  tying  it  there  close  to  the  valves,  and 
cutting  off  the  walls  of  the  vessel  above  the  ligature. 

Still  simpler  is  the  older  method  of  Baumgarten  (1843)  of  cutting  away  the  auricles 
to  expose  the  valves  and  then  pouring  in  water  from  a  beaker  (Fig.  14,  B). 

RELAXATION    OF   THE    HEART,  AND    TONICITY    OF    THE    CARDIAC    MUSCLE. 

It  has  been  supposed  by  some  writers  that  the  diastolic  dilatation  of 
the  heart  is  brought  about  by  some  active  muscular  contraction,  since  the 
pressure  within  both  ventricles  becomes  negative,  even  to  the  extent  of 
• —  55  mm.  Hg.  This  negative  pressure  is  of  only  momentary  duration,  and 
may  be  compared  to  that  occurring  within  a  rubber  ball  when  squeezed 
and  let  go.  The  walls  of  the  heart  are  sufficiently  rigid  and  are  sufficiently 
provided  with  elastic  fibres  to  resume  their  shape  like  a  rubber  ball,  and, 
on  the  other  hand,  the  pressure  in  the  coronary  arteries  tends  to  hold  them 
distended  as  though  by  a  wire  frame.' 

The  heart  muscle  is  quiescent  and  the  heart  walls  are  relaxed  during 
the  entire  period  of  diastole,  so  that  neither  the  most  delicate  recording- 
levers  nor  the  most  sensitive  galvanometers  reveal  the  slightest  signs  of 
contraction.  Nevertheless,  as  will  be  seen,  the  degree  of  this  diastolic  relax- 
ation of  the  walls  varies  considerably  under  different  circumstances  depend- 
ent upon  the  tonicity  of  the  heart  muscle.  This  is  shown  by  variations 
in  the  length  of  strips  of  cardiac  muscle  under  a  constant  load,  as  well  as 
b}'  variations  in  the  cardiac  volume. 

Tonicity. — T onicity  may  be  defined  as  the  resistance 
of  the  heart  muscle  to  stretching  in  diastole;  or,  less 
accurately,  as  its  diastolic  rigidity. 

The  force  which  stretches  the  heart  walls  in  diastole  is  the  pressure  at 
which  the  blood  enters  the  heart  from  the  great  veins,  namely  the  venous 
pressure,  so  that  with  a  high  venous  pressure  (unless  antagonized  by  a  high 
tonicity)  they  will  be  stretched  considerably  (dilatation),  while  with  a  low 
venous  pressure  comparatively  little  blood  will  enter  and  the  heart  will 
remain  small.  In  all  cases  filling  will  continue  until  an 
equilibrium  is  reached  between  the  venous  pressure 
and  the  cardiac  tonicity,  unless  the  heart  rate  is  so  rapid  that 
the  filling  is  interrupted  by  the  next  systole.  A  high  tonicity  will,  how- 
ever, antagonize  a  high  venous  pressure  and  prevent  overfilling. 

Moreover,  Howell  and  Donaldson  have  shown  that  the  systolic  output 
of  the  heart  depends  to  a  great  extent  upon  the  amount  entering  the  latter 
from  the  great  veins,  and  hence,  upon  the  venous  pressure.  If  the  venous 
pressure  falls  below  a  certain  level,  the  heart  fills  incompletely,  and  the  ven- 
tricles are  unable  to  pum.p  enough  blood  into  the  arteries  to  maintain  the 
blood-pressure  at  the  usual  level. 

The  rate  of  filling  of  the  heart  is  accelerated  (curve  of  filling  steeper) 
(Fig.  15)  when  either  the  venous  pressure  is  high  or  the  tonicity  is 
low;  the  filling  is  slowed  (curve  more  oblique)  when  either  the  tonicity  is 

'  For  a  detailed  account  of  the  various  theories  of  the  cardiac  relaxation,  with  full 
bibliography,  consult  E.  Ebstein,  Die  Diastole  des  Herzens,  Ergebnisse  der  Physiol., 
Wiesb.,  1904,  iii    2  Ahth. 


12 


DISEASES  OF  THE  HEART  AND   AORTA. 


high  or  the  venous  pressure  is  low.  So  that,  as  regards  filling  of  the  heart, 
a  high  tonicity  is  equivalent  to  a  low  venous  pressure,  and  conversely,  a 
low  tonicity  is  equivalent  to  a  high  venous  pressure  (Fig.  16). 

Influences  which  affect  tonicity  may  be  studied  objectively  in  i-solated 
strips  of  cardiac  muscle  by  means  of  their  shortening  or  lengthening,  or 
upon  the  intact  heart  by  changes 
in  the  volume  curve. 


Fig.  15. — Volume  curves  showing  the  effect 
of  variations  in  venous  pressure  ( V  P)  and  in  ton- 
icity {T)  upon  the  rate  at  which  the  ventricles  are 
filled  during  diastole. 


V  P  5cM. 


Fig.  16. — Volume  curves  showing  the  effect  of 
low  venous  pressure  or  of  high  tonicity  upon  the 
amount  of  blood  entering  the  ventricles.  (Modified 
from  Y.  Henderson.)  A  fall  in  the  venous  pressure 
is  equivalent  to  an  increased  tonicity.  CM,  centi- 
metres of  H2O  pressure. 


The  total  volume  of  the  heart  at  any  given  instant  may  be  regarded 
as  follows: 

Volume  of  heart  =  voluma  of  heart  walls  +  volume  of  blood  within  cardiac  chambers. 

Volume  of  walls  =  volume  of  muscle  +  coronary  blood  +  lymph.  (The  two  latter 
factors  vary  somewhat,  though  relatively  slightly,  the  lymph 
increasing  considerably  in  cardiac  stasis.) 

Volume  of  blood  within  chambers  =  output  at  each  systole  +  blood  remaining  at  end 
of  systole  (residual  blood). 

Residual  Blood. — The  residual  blood  undergoes  great 
variations.  In  dilated  hearts  it  may  attain  to  several  times  the 
amount  of  the  systolic  output  (cf.  Fig.  17),  while  in  small  hearts  it  may 
be  only  a  fraction  of  the  latter.  The  systolic  output,  on  the  other  hand, 
may  undergo  equally  large  variations. 


Fig.  17. — Diagram  to  illustrate  the  changes  in  volume  of  the  ventricles  in  systole  and  diastole 
associated  with  variations  in  tonicity  (7*)  and  systolic  output  (S.  O.).  N,  NORM.,  normal;  +,  increased; 
— ,  diminished.     Length  of  heavy  black  line  indicates  degree  of  tonicity. 

The  changes  in  tonicity  may  be  measured  by  the  volume  of  the  heart 
at  the  end  of  diastole,  i.e.  when  the  filling  is  most  complete,  a  large  diastolic 
volume  representing  low  tonicity  (when  venous  pressure  and  pulse-rate  are 
constant),  a  small  volume  indicating  a  high  tonicity. 

Nature  of  Changes  in  Tonicity. — Porter  l>as  found  that  a  strip  of  heart 
muscle  can  be  made  to  remain  elongated  (diminished  tone),  or  can  then  be 
made  to  remain  shortened  when  not  receiving  any  stimuli  whatever  (in- 
creased tone).     Several  degrees  of  this  permanent  shortening  can  be  super- 


PHYSIOLOGICAL  CONSIDERATIONS.  13 

posed  on  one  another  with  great  similarity  to  the  tetanus  of  skeletal  muscle 
("tetanus  of  tone,"  Porter).  Barcroft  and  Dixon  have  shown  that  the 
muscle  when  in  tone  gives  off  more  CO2  than  when  at  rest,  further  support- 
ing this  view  of  the  role  of  increase  and  decrease  in  tone. 

Factors  producing  Changes  in  Tonus. — F.  R.  Hoffmann  has  demon- 
strated that  there  are  two  separate  sets  of  fibres  in  the  frog's  vagus.  One  set 
influences  the  heart  rate  only  (chronotropic  effect),  the  other  increases  the 
size  and  force  of  contraction  (augmentor  effect)  and  also  increases  the 
cardiac  tonus  but  does  not  affect  the  rate  at  all.  This  group  of  fibres  is 
found  only  in  the  interauricular  and  interventricular  septum  (septal  nerves) 
in  the  frog.  In  other  animals  the  two  groups  of  fibres  pass  side  by  side  and 
cannot  be  dissociated,  though  it  is  frequent  in  weak  stimulation  of  the  vagus 
to  find  one  effect  occurring  without  the  other. 

P.  D.  Cameron,  in  the  writer's  laboratory,  has  found  that  in  dogs  the 
intravenous  administration  of  digitalis,  strophanthus,  nitroglycerin,  and 
calcium  salts  increases  cardiac  tonicity.  The  effect  of  small  (therapeutic) 
doses  of  these  drugs  is  exerted  almost  entirely  upon  the  tonic  fibres  in  the 
vagus,  and  fails  to  appear  if  the  vagi  have  been  cut  or  paralyzed  with  atro- 
pine. Larger  doses,  however,  exert  similar  effects  by  direct  action  on  the 
heart  muscle.  Atropine  itself  illustrates  these  effects  by  causing  a  primary 
depression  of  tonus  as  the  vagi  become  paralyzed,  which  is  followed  by  an 
increase  in  tonicity  from  direct  action  on  the  heart  muscle.  Potassium 
salts,  asphyxia,  formic  acid,  adrenalin  depress  tonicity.  Aconite  in  thera- 
peutic doses  affects  rate  more  than  tonus  in  the  dog. 

Since  the  exact  volume  of  the  heart  cannot  be  determined  clinically, 
the  area  of  the  cardiac  shadow  in  diastole  furnishes  the  best  index  of  the 
tonus,  especially  when  combined  with  study  of  the  venous  pressure.  Com- 
paratively little  investigation  has  been  carried  on  in  this  field.  Moritz  and 
Dietlen  have  shown  that  exercise  usually  increases  tonus  in  healthy  per- 
sons. The  study  of  tonus  has  also  proved  of  value  in  the  study  of  exercise 
and  in  the  controlling  of  hydrotherapy  and  drug  t;reatments,  as  well  as  in 
the  study  of  myocardial  insufficiency. 

ACTION   OF   THE   CARDIAC   NERVES. 

The  heart  rate  is  determined  by  action  of  the  vagus  and  accelerator 
nerves,  and  particularly  by  the  tonic  activity  of  the  centres  near  the  calamus 
scriptorius  of  the  medulla:  the  former  nerve  slows  the  heart  (inhibitory 
effect) ,  lowers  the  blood-pressure  (depressor  effect) ,  and  diminishes 
the  conductivity  (negatively  dromotropic  effect)  from  auricle 
(atrium)  to  ventricle;  the  latter  quickens  the  heart  (accelerator 
effect),  increases  the  force  of  the  contraction  and  cardiac  tonus 
(augmentor),  and  improves  conductivity  (Bayliss  and  Starling).  In 
some  cases  stimulation  of  the  accelerators  may  revive  a  heart  that  has 
ceased  to  beat  (Hering) . 

Both  vagi  and  accelerators  are  normally  in  tonic 
activity.  Reflex  quickening  of  the  pulse-rate,  as  from  emotion,  pain, 
sensation,  and  other  reflex  causes  (Reid  Hunt),  and  moderate  exercise 
(Hering  and  Bowen),  is  due  partly  to  diminution  of  tonic  activity  of  the 


14 


DISEASES  OF  THE  HEART  AND  AORTA. 


vagi,  partly  to  direct  stimulation  of  the  accelerators  (Hooker);  while  the 
acceleration  after  violent  exercise  is  due  to  stimulation  of  the  accelerators 
(Hering,  Bowen).  Acceleration  upon  mild  exercis3  can  also  be  obtained 
in  patients  whose  vagi  are  made  inactive  by  0.5  to  1.0  mg.  (yiir  to  eV'gr.) 
atropine  (Hirschfelder) .  On  the  other  hand,  exercise  caused  no  accelera- 
tion but  a  sUght  slowing  of  the  pulse  in  a  dog  from  which  Friedenthal  had 
removed  all  the  cardiac  nerves. 


;  -       '       (Till  and  cour-f  ■  :    ■    •  .  ■-..:.      ;  ■  :    •      .-    ,.^   ■   :    :    ■  :.     :  -      ,     •  ■  .^-ponding 

branches.  (Schematic;  modified  from  Dougla.s  Powell  and  Gibson.)  MOT  SENS,  nuclei  of  the  efferent 
(motor)  and  afferent  (sensory)  fibres  of  the  vagus;  C  1,  2,  3,  4,  5,  6,  7,  8,  and  T  1,  2,  3,  4,  5,  6,  7,  8, 
cervical  and  thoracic  (dorsal)  spinal  nerves  and  their  cutaneous  distribution;  SCG,  MCG,  ICG,  superior, 
middle,  and  inferior  cervical  ganglia;    REC  LAR,  recurrent  laryngeal  nerve;    C  PL,  cardiac  plexus. 


The  mode  of  action  of  the  cardiac  nerves  has  been  shrouded  in  mystery,  especially 
that  of  the  inhibition  by  the  vagus.  Howell  and  Duke  in  a  most  brilliant  series  of  researches 
have  shown  that  potassium  is  given  off  from  the  heart  muscle  and 
can  be  found  in  increased  quantity  in  the  perfusion  liquid  after 
the  vagus  has  been  stimulated.  Controls  without  vagus  stimulation  show 
no  such  increase.  It  would  therefore  appear  that  vagus  inhibition  is  a  true 
potassium  effect,  a  fact  further  borne  out  by  the  close  analogy  between 
the  action  of  this  element  and  stinmlation  of  the  vagus,  as  well  as  by  the  marked  increase 
in  the  action  of  the  vagus  after  the  administration  of  large  quantities  of  potassium  or 
after  increase  of  potassium  in  the  blood. 

These  observers  were  unable  to  demonstrate  any  effect  of  the  accelerators  upon  the 
liberation  of  calcium,  potassium,  or  nitrogen. 


PHYSIOLOGICAL  CONSIDERATIONS.  15 

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Greene,  C.  W. :  On  the  Relation  of  the  Inorganic  Salts  of  Blood  to  the  Automatic  Activity 
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Howell,  W.  H.:  The  Cause  of  the  Heart-beat,  J.  Am.  M.  Assoc,  Chicago,  1906,  xlvi,  Nos. 
22  and  23. 

Loeb,  J.:  Ueber  lonen  welche  rhythmische  Zuckungen  des  Skelettmuskels  hervorrufen, 
Beitrage  zur  Physiologic  (Festschr.  f.  A.  Fick),  Braunschweig,  1899,  p.  101.  The 
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Lingle,  D.  J.:  The  Action  of  Certain  Ions  on  Ventricular  Muscle,  Am.  J.  Physiol.,  Bost., 
1900,  iv,  265. 

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Langendorff,  O.:  Untersuchung  am  uberlebenden  Saugethierherzen,  Arch.  f.  d.  ges.  Phy- 
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d'Hallion,  M.:  Reviviscense  d'un  coeur  d'enfant  36  heures  apres  la  mort,  J.  d.  sc.  med.  de 
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Deneke,  Th.,  and  Adam,  H.:  Beobachtungen  am  isolirten  iiber  lebenden  menschlichen 
Herzen,  Ztschr.  f.  exper.  Path.  u.  Therap.,  Berl.,  1906,  ii,  491. 

Gaskell,  W.  H.:  On  the  Rhythm  of  the  Heart  of  the  Frog  and  the  Nature  of  the  Action 
of  the  Vagus  Nerve,  Phil.  Trans.  Roy.  Soc,  London,  1882,  p.  993.  On  the  Innerva- 
tion of  the  Heart,  with  Especial  Reference  to  the  Heart  of  the  Tortoise,  J.  Physiol., 
Cambridge,  1884,  iv,  43.  The  Contraction  of  Cardiac  Muscle,  Schafer's  Text-book  of 
Physiol.,  Edinb.  and  Lond.,  1900,  ii,  169. 

His,  W.,  Jun.:  Die  Thatigkeit  des  embryonalen  Herzens  und  deren  Bedeutung  fiir  die 
Lehre  von  der  Herzbewegung  beim  Erwachsenen,  Arb.  a.  d.  med.  Klin,  zu  Leipz., 
1893,  14. 

Bond,  G.  M. — Unpublished  experiments. 

Erlanger,  J.:  Irregularities  of  the  Heart  resulting  from  Disturbed  Conductivity,  Am.  J. 
M.  Sc,  Phila.,  1908,  n.  s.  cxxxv,  797. 

Keith,  A.,  and  Flack,  M.  W.:  The  Auriculoventricular  Bundle  of  the  Human  Heart,  Lan- 
cet, Lond.,  1906,  ii,  359. 

Keith,  A. :  An  Account  of  the  Structures  Concerned  in  the  Production  of  the  Jugular  Pulse, 
J.  Anat.  and  Physiol.,  Lond.,  1908,  xlii,  1. 


16  DISEASES  OF  THE  HEART  AND  AORTA. 

Retzer,  R.:  Some  Results  of  Recent  Investigations  on  the  Mammalian  Heart,  Anat.  Rec, 

Phila.,  190S,  ii,  149. 
Schonberg,  S.:  Ueber  Veranderungen  im  Sinusgebiet  des  Herzens  bei  chronischer  Arrhyth- 

mie,  Frankf.  Ztschr.  f.  Path.,  Wiesb.,  1908,  ii,  153. 
De  Witt,  L.  M. :  Observations  on  the  Sino-ventiicular  Connecting  System  of  the  Mammalian 

Heart,  Anat.  Rec,  Phila.,  1909,  iii,  475. 
McWilliam,  J.  A.:  On  the  Rhythm  of  the  Mammalian  Heart,  J.  Physiol.,  Camb.,  1888, 

ix,  167. 
Adam,  H.:  Experimentelle  Untersuchungen  ueber  den  Ausgangspunkt  der  automatischen 

Herzreize  beim  Warmbluter,  Arch.  f.  d.  ges.  Physiol.,  Bonn,  1906,  cxi,  607. 
Hering,    H.   E.:    Ueberleitungsstorungen    am    Saugethierherzen    mit  zeitwciiigem   Vor- 

hofssystolenausfall,    Ztschr.  f.  exper.    Path.    u.   Therap.,  Berl.,    1906,  iii,  511;   and 

Ueber  die  Automatic  des  Saugethierherzens,  Arch.  f.  d.  ges.  Physiol.,  Bonn,  1907, 

cxvi,  143. 
Hirschfelder,  A.  D.,and  Eyster,  J.  A.  E.:  Extrasystoles  in  the  Mammalian  Heart,  Am.  J. 

Physiol.,  Bost.,  1907,  xviii,  222. 
Langendorf,  O.,  and  Lehmann,  C:  Der  Versuch  von  Stannius  am  Warmbliiterherzen,  Arch. 

f.  d.  ges.  Physiol.,  Bonn,  1906,  cxii,  352. 
Fredericq,  L.:  La  pulsation  du  coeur  du  chien  est  une  onde  de  contraction  qui  debute  dans 

I'oreillette  droite,  etc.,  Arch,  internat.  de  physiol.,  Liege,  1906,  iv,  57. 
Lohmann,  A.:  Ueber  die  Funktion  der  Bruckenfasem,  an  Stelle  der  grossen  Venen  die 

Fiihrung  der  Herztatigkeit  beim  Saugetiere  zu  iibernehmen,  Arch.  f.  d.  ges.  Physiol., 

Bonn,  1908,  cxxiii,  628. 
Kent,  His,  Retzer,  Braunig,  Tawara.     See  Part  III,  Chapter  XI. 
King,  T.  W.    See  Part  HI,  Chapter  VII. 
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ser.  B,  vol.  Ixxxi,  151. 
Ludwig,  C:  Ueber  den  Bau  und  die  Bewegungen  der  Herzventrikel,  Ztschr.  f.  rat.  Med., 

Heidelb.,  1849,  vii,  189.  ; 
Krehl,  L.:    Beitrage   zur  Kenntniss  der  FuUung  und  Entleerung  des  Herzens,  Ahbandl. 

d.  Kgl.  sachs.  Gesellsch.  d.  Wissensch.,  Math.-phys.  Kl.,  Leipz.,  1891,  xvii,  341. 
MacCallum,  J.  B.:  On  the  Muscular  Architecture  and  Growth  of  the  Ventricles  of  the  Heart, 

Contrib.  Sc.  Med.  dedic.  to  W.  H.  Welch,  Baltimore,  1900,  307. 
Baumgarten,  A.:  Ueber  den  Mechanismus  durch  welchen  die  venosen  Herzklappen  gesch- 

lossen  werden.  Arch.  f.  Anat.,  Physiol,  u.  wissensch.  Med.,  Berl.,  1843,  463. 
Howell,  W.  H.,  and  Donaldson,  F.:  Experiments  upon  the  Heart  of  the  Dog,  Phil.  Tr.  Roy. 

Soc,  Lond.,  1884,  Part  I,  139. 
Henderson,  Y.  (with  the   collaboration   of    M.  McR.  Scarborough  and    F.  P.  Chilling- 
worth)  :  The  Volume  Curve  of  the  Ventricles  of  the  Mammalian  Heart  and  the  Signifi- 
cance of  this  Curve  in  Respect  to  the  Mechanics  of  the  Heart-beat  and  the  Filling  of 

the  Ventricles,  Am.  J.  Physiol.,  Bost.,  1906,  xvi,  325. 
Gad,  J.:  Klappenspiel  im  Ochsenherzen,  Arch.  f.  Physiol.,  Leipzig,  1886,  p.  380. 
Hooker,  D.  R.:  May  Reflex  Cardiac  Acceleration  Occur  Independently  of  the  Cardio-inhib- 

itory  Center?     Am.  J.  Physiol.,  Bost.,  1908,  xix,  417. 
Stewart,  H.  A.:  A  Clinical  and  Experimental  Study  of  the  Blood-pressure  and  Pulse  in 

Aortic  Insufficiency,  Thesis,  Edinb.,  1907;  also  Arch.  Int.  Med.,  Chicago,  1908,  i. 
Porter,  W.  T.:  Observations  on  the  Tonus  of  Heart  Muscle,  Am.  J.  Physiol.,  Bost.,  1906, 

XV,  1. 
Barcroft,  J.,  and  Dixon,  W.  E.:  The  Gaseous  Metabolism  of  the  Mammahan  Heart,  J. 

Physiol.,  Cambr.,  1907,  xxxv,  182. 
Hofmann,  Fr.:  L^eber  die  Function  der  Scheidewandnerven  des  Froschherzen,  Arch.  f.  d. 

•  ges.  Physiol.,  Bonn,  1895,  Ix,  139. 
Cameron,  P.  D.:  Physiological  and  Pharmacological  Studies  upon  the  Tonicity  of  the 

Mammalian  Heart,  Thesis,  Edinb.,  1908. 
Bayliss,  W.  M.,  and  Starling,  E.  H.:  On  Some  Points  in  the  Innervation  of  the  Mammalian 

Heart,  J.  Physiol.,  Camb.,  1892,  xiii,  407. 
Hunt,  Reid:  Direct  and  Refle.c  .Acceleration  of  the  Mammalian  Heart,  with  Some  Obser- 
vations upon  the  Relations  of  the  Inhibitory  and  Accelerator  Nerves,  Am.  J.  Physiol., 

Bost.,  1899,  ii,  395. 


PHYSIOLOGICAL  CONSIDERATIONS.  17 

Hering,  H.  E.:  Ueber  die  Beziehungen  der  extracardialen  Herznerven  zur  Steigerung  der 
Herzschalgzahl  bei  Muskeltatigkeit,  Arch.  f.  d.  ges.  Physiol.,  Bonn,  1895,  be,  429. 

Bowen,  W.  P.:  A  Study  of  the  Pulse-rate  in  Man  as  Modified  by  Muscular  Work,  Contrib. 
to  Med.  Research  (Vaughan),  Ann  Arbor,  1903,  p.  462. 

Hirschf elder,  A.  D.:  Observations  upon  Paroxysmal  Tachycardia,  Johns  Hopkins  Hosp. 
Bull.,  Bait.,  1906,  xvii,  337. 

Friedenthal,  H.:  Ueber  die  Entfernung  der  extracardialen  Herznerven  bei  Saugethieren., 
Arch.  f.  Physiol.,  Leipz.,  1902,  p.  135. 

Howell,  W.  H.,  and  Duke,  W.  W.:  The  Effect  of  Vagus  Inhibition  on  the  Output  of  Potas- 
sium from  the  Heart,  Am.  J.  Physiol.,  Bost.,  1908,  xxi,  51.  Note  upon  the  Effect 
of  Stimulation  of  the  Accelerator  Nerve  upon  the  Calcium,  Potassium,  and  Nitrogen 
Metabolism  of  the  Isolated  Heart,  ibid.,  1908-1909,  xxiii,  174. 


II. 

BLOOD-PRESSURE  AND  BLOOD  VISCOSITY. 

THE  BLOOD-PRESSURE  IN  HEALTH  AND  DISEASE. 

Definition. — The  blood-pressure,  or  "arterial  tension,"  is  the  pressure 
which  the  blood  is  exerting  upon  the  walls  of  the  vessel  in  which  it  is  to 
be  measured  (lateral  pressure),  or  upon  the  column  of  blood  ahead  of  it 
in  the  direction  in  which  it  is  flowing  (end  pressure) . 

The  end  pressure  is  equal  to  lateral  pressure  —  velocity  head,  but  as  a  rule  differs 
by  only  a  few  millimetres  from  the  lateral  pressure.  The  end  pressure  in  the  branch  of  a 
vessel  is  equal  to  the  lateral  pressure  in  the  vessel  from  which  it  branches. 


Fig.  19. — Curve  of  intraventricular  and  aortic  pressures.  (After  Huerthle.)  .4 ,  aortic  pressure ; 
V,  intraventricular  pressure;  D,  curve,  taken  with  a  differential  manometer,  showing  the  differences  of 
pressure  between  left  ventricle  and  aorta. 


Pressure  within  the  Left  Ventricle. — It  is  evident  that  in  a  system  of 
elastic  tubes  like  the  arteries,  the  pressure  of  the  blood  in  any  segment  of 
artery  is  brought  about  by  the  tendency  of  the  inflow  (from  the  heart)  to 
remain  in  excess  of  the  outflow  through  the  capillaries.  The  inflow  to  the 
arteries  is  maintained  by  the  pumping  action  of  the  heart,  that  is,  by  the 
intraventricular  pressure  during  systole.  As  shown  by  Huerthle  and  Porter 
the  pressure  within  the  ventricle  remains  tolerably  constant  throughout 
systole  and  takes  the  form  of  a  plateau  more  or  less  independent  of  the  pulse 
curve  in  the  aorta  (Fig.  19),  though  the  floor  of  the  plateau  slopes  down- 
ward with  peripheral  dilatation  and  upward  with  constriction. 

If  the  systole  is  too  weak  to  open  the  aortic  valves,  and  the  heart 
contracts  without  change  in  volume  (isometrically),  the  curve  does  not 
remain  a  plateau,  but  has  a  rounded  apex  like  that  of  the  isometric  con- 
traction of  skeletal  muscle.  The  pressure  within  the  ventricle  when  the 
18 


BLOOD-PRESSURE   AXD    BLOOD   VISCOSITY.  19 

aortic  valves  are  open  is  slightly  in  excess  of  that  within  the  aorta,  that 
is,  very  little  above  the  maximal  pressure  as  measured  in  the  latter,  and  it 
remains  at  this  height  until  the  end  of  systole,  when  the  aortic  valves  close. 

Huerthle  and  others  have  shown  that  the  intraventricular  pressure  is  not  alwaj^s 
constant  throughout  systole,  but  that  when  the  peripheral  resistance  is  very  low  it  falls 
toward  the  end  of  systole,  while  if  the  peripheral  resistance  is  very  high  it  rises  toward  the 
end  of  systole. 

The  Maximal,  Minimal,  and  Pulse  Pressures. — Accordingly,  when  the 
aortic  valves  open  (.07  to  .09  second)  after  the  beginning  of  ventricular 
systole  (see  Fig.  45,  page  53),  the  pressure  in  the  aorta  soon  rises  to  its 
maximum,  and  from  that  time  until  the  beginning  of  the  next  systole 
it  diminishes  more  or  less  gradually  as  the  excess  of  blood  flows  out  from  the 
arterial  tree  through  the  capillaries  and  into  the  veins.  The  minimal 
pressure  is  reached  just  before  the  beginning  of  the  next  systole.  The 
pulse-pressure  is  the  difference  between  the  maxi- 
mal  and    minimal   pressures. 

Characteristics  of  the  Pulse. — It  is  evident  that  the  maintenance  of 
the  circulation  depends  upon  the  head  of  pressure  in  the  arteries,  and 
accordingly  much  attention  was  paid  by  the  older  clinicians  to  the  "  arterial 
tension"  and  the  "quality  of  the  pulse,"  which  they  thought  were  mani- 
festations of  it.  The  arterial  tension  was  judged  by  the  force  necessary 
to  obliterate  the  pulse  at  the  wrist  when  the  fingers  are  pressed  upon  the 
radial  artery.' 

A  still  more  accurate  method  of  feeling  the  pulse  is  to  empty  the  artery  for  a  few 
centimetres  by  "milking"  out  the  blood  with  two  fingers  of  one  hand,  while  obliterating 
the  artery  above  the  wrist  with  the  fingers  of  the  other  hand.  The  pressure  of  the  latter  is 
then  gradually  diminished  until  the  return  of  the  pulse  is  felt,  this  point  marking  the  m  a  x  i- 
m  a  1  or  systolic  pressure.  By  careful  training  of  the  sensations  and  comparing  the  observa- 
tion with  the  results  of  a  good  sphygmomanometric  determination  made  at  the  same  time, 
a  great  degree  of  skill  in  judging  pressures  may  be  attained;  one  of  the  writer's  teachers, 
who  has  cultivated  this  perception  to  a  remarkable  degree,  voices  the  general  experience 
in  saying,  "I  can  estimate  the  blood-pressure  with  the  fingers  alone  quite  accurately  in 
about  eight  cases  out  of  ten,  but  those  in  which  it  is  of  real  importance  are  always  the 
other  two. " 

The  minimal  pressure  may  also  be  judged,  but  even  less  accurately,  by  estimating 
the  amount  of  pressure  at  which  the  size  of  the  pulse  just  begins  to  decrease  as  one  raises 
the  pressure  in  the  artery. 

Determination  of  Maximal  Blood=pressure. — Instruments  for  determine 
ing  the  blood-pressure  date  from  1855,  w^hen  K.  Vierordt  determined  the 
weight  that  could  be  placed  over  the  radial  artery  before  the  pulse  was 
obliterated. 

Marey  (1876)  devised  the  first  useful  apparatus  for  estimating  the  blood-pressure  in 
man.  He  placed  the  hand  in  a  plethysmograph  connected  with  a  bottle  for  raising  the 
pressure  and  a  sphygmoscope  tambour  for  recording  the  size  of  the  pulse-waves.  He  states 
(1878)  that  the  maximal  pressure  may  be  determined  as  the  point  where  the  pulsation 
disappears,  the  minimal  as  the  point  where  the  oscillations  are  largest.  It  is  worthy  of 
note  that  Marey  was  twenty-five  years  in  advance  of  the  times,  and  that  his  methods 
and  conclusions  are  almost  exactly  those  of  the  best  modern  methods  (Erlanger  and  v. 
Recklinghausen).  Unfortunately,  the  work  of  Marey  was  little  knoiyn,  and  the  first 
apparatus  to  attain  general  use  was  that  of  v.  Basch  (1887).  Unlike  Marey,  v.  Basch 
studied  only  the  maximal  pressures,  but  much  good  pioneer  work  was  done  with  this 


20 


DISEASES   OF  THE   HEART   AND   AORTA. 


instrument.  It  consisted  of  a  small  rubber  bulb  filled  with  water  and  communicating  with 
a  mercury  manometer.  The  bulb  was  pressed  upon  the  radial  artery  until  the  pulse  below 
it  was  obliterated,  and  the  pressure  necessary  was  read  off  upon  the  manometer.  V.  Basch 
modified  the  apparatus  later  by  using  a  spring  manometer,  and  Potain  substituted  air 
for  water  in  the  bag  with  an  aneroid  barometer.  This  method  is  still  almost  universal 
in  France,  but  the  possible  error  with  v.  Basch's  as  well  as  Potain's  methods  is  as  much  as 
78  mm.  Hg  (Tigerstedt) . 

Riva-Rocci  (1896)  and  L.  Hill  and  H.  Barnard  (1897)  introduced  the 
use  of  a  rubber  bag  about  the  upper  arm,  surrounded  by  a  non-elastic  cuff 
of  silk  (Riva-Rocci)  or  of  leather  (Hill  and  Barnard)  instead  of  the  small 
bag  that  Potain  pressed  upon  the  artery,  and  they 
compressed  the  artery  with  pressure  from  an  air- 
pump  or  Davidson  syringe,  feeling  the  return  of  the 
pulse  at  the  wrist  as  the  air  was  allowed  to  escape 
and  reading  off  the  pressure  corresponding.  These 
are  the  methods  now  in  most  general  use,  the  only 
modification  being  that  the  rubber  bag  must  not  be 
less  than  12  cm.  in  diameter  instead  of  5  cm,  as  used 
by  Riva-Rocci;  for  v.  Recklinghausen  has  shown  that 
with  narrow  cuffs  a  great  deal  of  pressure  is  lost  in 
squeezing  the  tissues,  and  hence  the  readings  obtained 
with  them  are  too  high,  but  this  is  now  remedied  by 
using  the  broad  cuff.  Riva-Rocci's  method  was  used 
only  for  determining  the  maximal  pressure. 

However,  Marey  (I.e.)  had  shown 
that  the  maximal  pulse-wave  was  ob- 
tained when  the  pres- 
sure about  an  organ 
was  equal  to  the  pres- 
sure within  the  artery 
supplying  it  (i.e.,  the 
minimal  pressure  —  Howell 
and  Brush) ,  and  this  observa- 
tion furnished  a  basis  for  such 
determinations  in  mar. 

Determination  of  Mini= 
mal  Blood  =  pressure.  —  Nu- 
merous methods  for  determining  the  minimal  blood-pressure  have 
been  devised,  especially  those  of  Hill  and  Barnard,  and  Mosso,  but  those 
which  are  useful  and  I'eliable  in  practice  date  from  1901,  when  Masing 
began  to  determine  minimal  pressure  by  the  point  at  which  the  radial 
pulse  seemed  to  become  largest.  About  the  same  time  Jane  way  esti- 
mated the  minimal  pressure  at  the  point  where  the 
oscillations  of  the  mercury  column  in  the  manom- 
eter seemed  greatest.  This  is  a  satisfactory  method  in  most 
cases,  but  the  judgment  by  the  eye  is  sometimes  difficult  and  in  small 
pulses  may  be  impossible. 

In  1904  Strasburger  revived  Masing's  method,  as  did  also  Sahli,  who  recorded 
the  maximal  pulse-wave  with  a  sphygmograph  at  the  wrist.  The  latter  method  is 
very   cumbersome.     For   practical    purposes    the   method   of   Masing   and   Strasburger 


Fig.  20. — Riva-Rocci  blood -pressure  apparatus  as  modified 
by  Stanton.     (Kindness  of  the  A.  H.  Thomas  Co.) 


BLOOD-PRESSURE  AND   BLOOD   VISCOSITY. 


21 


Fig.  21. — Correct  method 
of  feeling  the  pulse  in  Stras- 
burger's  determination  of  mini- 
mal pressure. 


is  fairly  satisfactory,  provided  a  few  precautions  are  taken.  First,  it  is  necessary 
to  exert  an  absolutely  uniform  pressure  with  the  fingers  upon  the  radial  artery 
throughout  the  determination.  Ordinarily  this  is  very  difficult  ;  but  if  the 
artery  is  palpated  with  the  ball  of  the 
finger  instead  of  the  finger-tips,  while 
the  finger-tips  rest  against  the  radius, 
as  shown  in  the  figure  (Fig.  21),  any  changes  of  pres- 
sure by  the  fingers  are  exerted  against  the  bone  and 
not  against  the  artery,  and  a  very  uniform  pressure 
is  exerted  upon  the  latter.  Secondly,  it  is  necessary 
to  raise  and  then  gradually  let  out  the  pressure  from  the 
bag  while  feeling  the  pulse  in  this  way,  in  order  to 
acquaint  oneself  with  the  changes  of  pulse  to  be  expected. 
Thirdly,  it  is  necessary  to  repeat  the  determination 
four  to  six  times  in  order  to  eliminate  the  great  discrep- 
ancies that  creep  in  when  single  readings  are  made. 
All    the   non-concordant    readings  should   be  disregarded. 

In    this    way   fairly   accurate   determinations    of   minimal    pressure   may   be    obtained 
(within    5   mm.    of   those   obtained    by   Erlanger's    apparatus). 

Erlanger's  Sphygmomanometer. — The  most  accurate  and  sat- 
isfactory, if  somewhat  bulky,  sphygmomanometer  is  that  of  Erlanger 
with  which  graphic  records  of  both  maximal  and  minimal  pressures  may 
be  obtained  (Fig.  22).     Erlanger's  apparatus  differs  from  the  Riva-Rocci 

with  Recklinghausen  cuff  only  in 
the  fact  that  by  means  of  a  T-tube 
the  cuff  is  connected  also  with  a 
rubber  pressure-bag  in  a  glass  case. 
The  oscillations  of  pressure  in  the 
cuff  are  thus  communicated  to  the 
pressure  bag,  and  the  oscillations 
of  this  bag  are  communicated  to 
the  air  in  the  glass  case  around  it, 
and  are  recorded  by  the  movements 
of  a  Marey  tambour  upon  the  smoked 
paper  on  a  small  drum.  He  is  also 
able  to  let  the  pressure  flow  out 
very  slowly  by  a  series  of  capillary 
outlets  of  different  bores.  A  com- 
plicated stop-cock  allows  any  of 
these  to  be  used  at  will. 

In  using  the  Erlanger  apparatus,  one 
turns  the  stop-cock  to  the  point  marked 
"In,"  then  raises  the  pressure  in  the  bag 
to  well  above  the  maximum  arterial  pres- 
sure, and  turns  the  stop-cock  to  the  point 
marked  1  or  2,  which  corresponds  to  capil- 
lary outlets  of  different  sizes.  The  pressure 
in  the  bag  falls  gradually,  and  soon  small 
oscillations  of  the  lever  are  seen,  due  to  the  impact  of  the  compressed  artery  upon  the  upper 
margin  of  the  bag.  A  sudden  increase  in  the  size  of  these  wavelets  soon  takes  place  and  marks 
the  maximal  pressure,  which  is  read  off  on  the  manometer;  it  is  just  a  trifle  below  the  maxi- 
mal pressure  that  the  first  pulse- wave  passes  completely  through  under  the  cuff  and  causes 
the  larger  wave,  upon  which  also  a  small  shoulder  is  usually  seen.  Below  this  point  the  oscil- 
lations continue  to  increase  in  size  and  then  begin  to  decrease,  the  manometer  being  watched 


Fig.  22. — Erlanger  blood-pressure  apparatus 
with  Hirschfelder  polygraph  attachment.  (Kind- 
ness of  Schneider  Bros.) 


22 


DISEASES   OF   THE    HEART    AND    AORTA. 


all  the  while.  The  point  at  which  the  oscillations  are  maximal  is  the  minimal  or 
diastolic  blood-pressure.  Sometimes,  especially  in  arteriosclerotics,  the  oscilla- 
tions decrease  a  little  and  then  again  increase  at  about  10  mm.  lower  pressure.  In  that 
case  Erlanger  has  shown  that  the  lower  point  or  second  maximum  of  oscil- 
lations is  the  one  corresponding  to  the 
minimal   pressure. 

In  order  to  keep  these  records  per- 
manent Fontaine  marks  off  on  the  drum 
the  points  which  correspond  to  each  fall 
of  5  or  10  mm.  Hg  in  the  manometer. 
These  marks  are  made  by  means  of  one 


J 

, 

\,^^ 

iiipi 

4   . 

M 

\           VlAX 

>im. 

\\5 

ss 

Fig.   23. — Diagram    showing    arrangement    of 
Erlanger   apparatus.      (After   Howell.) 


Fig.  24. — Curve  taken  with  the  Erlanger 
blood-pressure  apparatus,  showing  the  points  of 
maximal  and  minimal  pressures. 


of   the    tambours  upon  the   polygraph   (Hirschfelder)    attachment   which  is  caused  to 
vibrate  by  squeezing  a  small  pipette  inserted  into  the  long  rubber  tube. 

This  apparatus  has  been  carefully  tested,  both  upon  animals  and  upon  mechanical 
models,  and  has  been  shown  to  give  accurate  results.  Of  course  it  cannot  be  used  unless 
the  muscles  of  the  arm  are  at  rest,  but  neither  can  any  other  sphygmomanometer,  without 
introducing  a  large  error.  The  readings  ob- 
tained in  determining  both  maximal  and  mini- 
mal pressures  in  arteriosclerotics  are  too  high, 
but  this  error  is  also  universal  and  at  present 
unavoidable.  At  times  the  systolic  increase 
in  size  is  not  sudden,  but  this  can  usually  be 
remedied  by  pressing  the  lever  a  little  more 
tightly  than  before  against  the  drum.  Occa- 
sionally a  larger  or  smaller  capillary  outlet 
is  required  and  these  may  be  readjusted. 
The  readings  obtained  by  Erlanger's  method 
are,  as  a  rule,  about  5  mm.  higher  for  the 
maximal  (systolic)  pressure  than  by  the 
broad  cuff  Riva-Rocci,  and  for  the  minimal 
(diastolic)  within  about  5  to  10  mm.  of  the 
readings  by  the  method  of  Masing  and 
Strasburger  as  modified  by  the  writer  (Hirsch- 
felder,  also  Brush).  Erlanger's  method 
gives  results  sufficiently  unequivocal  to 
form  the  basis  for  a  research,  although  the  other  method  is  often  quite  satisfactory-. 

V.  Recklinghausen's  Sphygmotonometer.  —  Numerous  other  sphygmomanometers 
have  been  devised  of  late,  notably  the  sphygmoscope  of  Pal  for  visual  deter- 
mination of  pressure  by  the  movement  of  a  drop  of  colored  liquid,  and  the  visual 
(tonometer)  and  graphic  (tonograph)  methods  of  v.  Recklinghausen,  upon  the  same 
principle  as  Erlanger's,  but  they  do  not  possess  any  special  advantages  in  their  respective 
spheres  of  usefulness  over  the  methods  given  above. 


Fic;.  25.  —  v.  Recklinghausen  apparatus. 
(After  V.  Recklinghausen,  Arch.  f.  exper.  Path.  u. 
Pharmacol.,  Iv.) 


BLOOD-PRESSURE   AND    BLOOD   VISCOSITY.  23 

Auscultatory  Method  for  Determination  of  the  Blood-Pressures. — A  very  ingenious 
method  for  determining  the  maximal  and  minimal  blood-pressures  was  devised  by 
Korotkoff  in  1905.  If  the  pressure  in  a  rubber  cuff  upon  the  upper  arm  is  allowed  to 
fall  gradually  from  a  point  above  the  maximal  arterial  pressure,  while  the  observer  listens 
with  a  stethoscope  pressed  upon  the  brachial  artery  at  a  point  about  two  centimeters 
below  the  lower  border  of  the  cuff,  no  sound  will  be  heard  until  as  soon  as  the  pressure 
in  the  cuff  falls  below  the  maximal  arterial  pressure.  As  the  minimal  arterial  pressure 
is  approached,  the  second  sound  also  becomes  louder,  reaches  its  maximum  at  the 
minimal  arterial  pressure  (where  there  is  the  greatest  alternate  expansion  and  con- 
traction of  the  artery),  and  disappears  rapidly  when  the  pressure  in  the  cuff  is  a  trifle 
below  the  minimal  (diastolic)  pressure.  Indeed,  Fellner  has  found  this  method  accurate 
to  within  5-10  mm.  Hg  of  the  readings  with  the  v.  Recklinghausen  apparatus.  Miss  Allen 
and  Mr.  Engle,  in  the  study  of  the  blood-pressures  of  35  patients  in  the  Johns  Hopkins 
Hospital,  found  that  the  readings  by  this  method  never  differed  more  than  2-5  mm.  from 
control  determinations  made  at  the  same  time  with  the  Erlanger  apparatus,  though  they 
took  the  minimal  pressure  at  the  point  at  which  the  second  sound  absolutely  disappeared. 

The  method  seems  therefore  to  be  one  of  considerable  accuracy,  though  in  persons 
with  very  small  vessels  it  may  be  difficult  or  impossible  to  use. 

Pocket  Form  of  BIood=Pressure  Apparatus. — The  exigencies  of  the  busy  practitioner 
demand  an  apparatus  to  occupy  small  space  and  yet  give  results  of  reasonable  accuracy. 
To  this  end  Potain  made  use  of  a  small  dial  upon  which  the  pressure  was  shown  by  the 
compression  of  a  spring  calibrated  in  centimetres  of  mercury.  More  recently  a  number 
of  such  forms  have  been  devised  in  which  the  pressure  chamber  is  connected  with  the 
usual  Riva-Roci-Recklinghausen  cuff.  The  Tycos  apparatus  represents  one  of  the  most 
compact  of  these.  It  is  practically  a  miniature  v.  Recklinghausen  sphygmotonometer, 
packed  so  small  that  it  may  be  carried  in  the  pocket  with  ease.  The  readings  are  made 
by  the  same  method  as  upon  the  v.  Recklinghausen,  but  the  excursions  are  much  smaller, 
a  fact  which  often  interferes  with  the  determination  of  minimal  pressure.  Nevertheless, 
Messrs.  Engle  and  Dandy,  in  the  Johns  Hopkins  Medical  Clinic,  have  found  that  determi- 
nations with  this  apparatus  usually  approach  within  5-10  mm.  of  the  determinations 
with  the  Erlanger  apparatus.  This  error  is  usually  due  to  the  fact  that  the  maximal 
pressure  is  determined  by  digital  palpation,  in  which  there  is  an  inherent  error  of  about 
this  amount,  regardless  of  the  form  of  apparatus  used.  The  determinations  of  minimal 
pressure  usually  fell  within  5  mm.  of  those  made  with  the  Erlanger. 

When  the  readings  were  made  by  the  auscultatory  method  it  was  possible  to  reach 
absolute  accuracy  in  many  cases  with  this  pocket  form  of  apparatus.  Like  all  spring 
pressure  gauges,  this  spring  is  liable  to  wear  out  in  time,  so  that  it  should  be  controlled 
every  few  months  by  comparison  with  a  mercury  manometer  at  various  points  through- 
out the  range  of  pressure. 

Gibson's  Sphygmomanometer. — Still  more  recently  Gibson  and  Sahli  have  devised 
an  apparatus  similar  to  Erlanger's  but  recording  the  oscillations  of  the  mercury  manome- 
ters directly  by  a  float  instead  of  by  the  Marey  tambour.  These  instruments  give  results 
fairly  concordant  with  the  Erlanger  and  have  the  advantage  of  recording  the  corresponding 
pressure  directly  in  absolute  figures. 

Normal  Blood-pressures. — For  young  persons  (19  to  25  years  old)  in  the  reclining 
posture  the  average  blood-pressure  according  to  Erlanger  is  maximal  110  mm.,  minimal 
65  mm.,  pulse-pressure  45  mm.  In  general  the  limits  in  normal  individuals  at  rest  are 
maximal  110  to  135  mm.,  minimal  60  to  90  mm.,  pulse-pressure  30  to  45  mm.  In  the 
experience  of  the  writer  a  maximal  pressure  of  115  to  120  mm.,  with  a  minimal  of  75  to 
85  mm.,  pulse-pressure  30  to  40,  is  more  common. 

MECHANISM    OF    THE    CIRCULATION. 

Pressure  in  Different  Parts  of  the  Vascular  System.- — Dawson  has  shown 
that  the  mean  pressure  is  very  constant  throughout  the  arterial  system, 
while  the  maximal  pressure  falls  greatly  as  one  approaches  the  periphery. 
The  minimal  pressure  is  also  quite  constant.  As  one  approaches  the  periph- 
ery the  maximal  pressure  falls  quite  rapidly  to  meet  the  minimal,  and  in 
the  smallest  arteries  they  are  practically  equal.     Hence  the  pressure 


24 


DISEASES   OF   THE   HEART   AND   AORTA. 


in  these  arterioles  does  not  differ  greatly  from 
the  minimal  pressure  in  the  aorta,  although  it  is  certainly 
a  few  millimetres  less.  The  minimal  arterial  blood-press- 
ure therefore  represents  the  perii)heral  resistance 
(vasomotor  changes),  while  the  maximal  pressure  approxi- 
mates the  intraventricular  pressure.  Marey  (I.e.)  has 
shown  that  this  approximation  is  closest  when  peripheral  resistance  is 
high.  Accordingly  the  pulse-pressure,  or  difference  between  the  two, 
represents  the  head  of  pressure  tending  to  drive  the  blood  from  the  heart 
through  the  aorta  and  large  arteries  onward  into  the  peripheral  arterioles. 
The  fall  in  pressure  may  be  compared  to  a  cascade 
whose  first  descent  is  from  heart  to  arterioles, 
whose  second  from  arterioles  to  capillaries,  and  whose 
third  is  from  the  capillaries  back  to  the  heart.  The 
actual  head  of  pressure  at  any  point  in  the  arteries  is  never  equal  to 
the  total  head  (maximal  pressure)  which  would  be  active  if  the  fall 
were  uninterrupted  by  interposed  resistance,  but  is  more  nearly  equal 
to  the  pulse-pressure. 

FACTORS    DETERMINING    MAXIMAL    AND    MINIMAL    PRESSURE. 

The  fall  in  blood-pressure  during  diastole  continues  until  the  next 
systole  takes  place.  If  the  pulse-rate  is  rapid  the  diastole  is  short  and  the 
blood-pressure  has  not  time  to  fall  much;  hence,  other  things  being  equal, 
minimal  pressure  rises  and  p  u  1  s  e  -  p  r  e  s  s  u  r  e  falls  as 
pulse-rate   increases. 


Fig.  26. — Diagram  showing  the  maximal  and  minimal  pressures  in  various  parts  of  the  circulatory  system. 


Erianger  and  Hooker  have  claimed  that  under  ordinary  conditions  the  product  of 
pulse-pressure  multiplied  by  pulse-rate  is  tolerably  constant, 
and  represents  roughly  the  velocity  of  blood  flow,  although  Y.  Henderson,  the  writer, 
and  others  have  proved  that  this  is  very  inaccurate  and  may  involve  an  error  of  more  than 


BLOOD-PRESSURE   AND   BLOOD   VISCOSITY. 


25 


50  per  cent.  The  curves  of  Dawson  and  Gorham,  who  claim  that  the  pulse-pressure  is  a 
"reliable  index"  of  the  systolic  output  (per  beat)  of  the  ventricles,  indicate  that  these 
writers  referred  to  quahtative  rather  than  quantitative  changes.  Henderson  has  show'n, 
however,  that  within  a  certain  range  of  pulse-rate  the  ventricular  output  per  beat  varies 
inversely  as  the  pulse-rate.  Within  this,  the  usual,  range  the  velocity  of  blood  flow  is 
greatest.  At  rates  below  it  time  is  lost  during  the  periods  of  diastasis;  above  it  the  suc- 
cessive systoles  encroach  upon  the  period  of  ventricular  filling  and  cut  short  the  inflow. 
Within  the  limits  indicated  by  Henderson,  Erlanger  and  Hooker's  index  of  velocity  may 
often  be  correct,  especially  when  there  are  no  extreme  vasomotor  changes. 


170 

II 

tfie 

11 

150 

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Fig.  27. — Diagram  showing  effects  of  vasoconstriction,  vasodilation,  increased  and  decreased  force 
of  ventricular  contraction  upon  the  maximal  and  minimal  blood-pressures  and  upon  the  form  of  the  pulse. 
SYS,  sy.stole;    DIAS,  diastole;    ART,  large  arteries;    AOL,  arterioles;    CAP,  capillaries. 

If  the  peripheral  vessels  dilate,  more  blood  can  flow  through  in  the  same  time,  and 
hence  when  the  pulse-rate  is  constant,  vasodilation  brings  about  fall  in 
minimal  pressure,  rise  in  pulse-pressure;  vasoconstriction 
brings  about  rise  in  minimal  pressure,  fall  in  pulse-pressure, 
but  a  change  in  maximal  pressure  following  the  change  in  minimal  usually  occurs  reflexly. 
Figure  26  shows  the  various  relations  of  maximal,  minimal,  and  pulse-pressures  to  the 
state  of  the  intraventricular  pressure. 

Erlanger  and  Hooker  give  the  following  table  to  indicate  the  conditions  present  in 
the  circulatory  system;  but  owing  to  the  inaccuracy  of  the  calculations  this  furnishes  use- 
ful information  only  when  the  changes  are  extremely  marked. 


Minimal  (mean) 
blood-pressure. 

Pulse-pressure  X  pulse- 
rate  velocity. 

Energy  of  heart. 

Peripheral  resistance. 

Constant \ 

} 

Increased 

Diminished 

Diminished 

Increased 

Unchanged ,. - 

Increased 

Increased < 

Increased 

Unchanged 

Unchanged 

Increased 

f 

Diminished 

Diminished 

Diminished < 

Unchanged 

Diminished 

Increased 

Unchanged 

Changes  in  the  peripheral  vessels  can  be  recorded  by  placing  the  patient's  hand  in  a 
plethysmograph  (Fig.  28)  which  is  sealed  hermetically  about  the  forearm  by  means  of  a 
rubber  cuff.  The  free  space  in  the  plethysmograph  is  filled  with  water,  which  runs  in  or 
siphons  out  of  a  tube  leading  to  a  movable  test-tube.  Changes  in  volume  of  the  arm  are 
recorded  by  upward  or  downward  movements  of  the  test-tube. 


26 


DISEASES   OF   THE   HEART    AND    AORTA. 


Work  of  the  Heart. — Since  the  intraventricular  pressure  is  almost  con- 
stant throvighout  systole,  it  is  evident  that  the  work  done  by  the  heart  is 
tolerably  constant  throughout  this  period;  and  since  no  work  is  done  during 
diastole,  it  is  evident  that  the  work  of  the  heart  per  minute  may  be  esti- 
mated, at  least  roughly,  by  the  product  of  intraventricular  pressure  X  dura- 
tion of  systole  X  pulse-rate.' 


Fig.  28. — Mosso  plethysmograph .  (After  Howell.)  a,  cylinder  of  plethysmograph;  t,  water  in 
recording  test-tube,  which  moves  by  extensioH  of  spring  a  (spring  s  is  arranged  of  a  strength  that  keeps 
water  in  <  at  a  constant  level);   p,  point  recording  the  excursions  of  test-tube  t. 

The  vaJue  of  blood-pressure  determinations  as  an  inde.x  of  the  func- 
tional power  of  the  heart  will  be  discussed  on  page  142  in  relation  to  exercise 
and  cardiac  overstrain. 


VARIATIONS  IN  BLOOD-PRESSURE  UNDER  PHYSIOLOGICAL 
CONDITIONS. 

1.  Change  of  position.  Erlanger  and  Hooker  have  shown  that  the  minimal 
pressure  usually  rises  considerably  and  the  pulse-pressure  always  decrease. s 
upon  standing  after  having  lain  down.    The  pulse-rate  increases  accordingly.    They  have 

'shown  that  these  effects  are  entirely  due  to  the  rule  of  gravity. 

2.  After  meals  the  maximal  pressure  and  pulse-pressure  are 
increased,  also  the  pulse-rate,  and  the  minimal  pressure  may  be  increased  but  to  a 
less  extent.    The  circulation  is  accelerated. 

3.  After  exercise  the  effect  is  the  same  as  after  meals,  only  more  marked.  When 
exercise  is  continued  to  the  point  of  fatigue  the  pressures  fall,  the  pulse-rate  falls  also,  and 
the  circulation  is  slowed  (Schott,  Masing,  Cabot,  Bowen).      (See  page  131.) 


'  For  more  complicated  and  perhaps  more  accurate  formulae  cf.  Tigerstedt  (1.  c). 

.  Pulse-pressure 

The  ratio  — — ; t—. — t^t or  Blood-pressure  coeincient  is  used  more  or 

Maximal  (systolic)  pressure 

less  as  an  index  of  circulatory  conditions.    Its  significance  may  be  given  as  follows: 

P.  P.  X  P.  Rate  =Velocity  )      ^^  .  ,  ,       ,  ,  i  •  ..• 

S^rstTPT^PTHate^  Work  [  =  Efficiency  of  heart  as  a  pump.     In  a  normal  indi- 

vidual  this  coefficient  is  25  per  cent,  to  35  per  cent. 


BLOOD-PRESSURE  AND   BLOOD   VISCOSITY. 


27 


4.  Upon  sensory  stimulation  the  vasomotor  centre  in  the  medulla  usu- 
ally responds  by  constricting  the  peripheral  vessels,  anil  the  pressure,  especially  the  mini- 
mal pressure,  rises.  The  pulse-rate  usually  quickens  also.  There  are  great  variations 
in  the  response  of  different  healthy  individuals  to  pain  sensations.  Dr.  A.  Berg,  under  the 
writer's  direction,  has  tested  the  effect  of  pinching  the  ear  upon  the  blood-pressure  of  healthy 
individuals,  and  has  found  in  some  persons  a  rise  of  blood -pressure  amounting 
to  10  to  20  mm.  Hg,  in  others  no  effect,  in  others  a  fall  of  about  10  mm.  Too  intense 
stimuli  produce  shock.  Mental  exertion  has  a  similar  effect — a  definite  vasocon- 
striction setting  in,  which  is  shown  by  the  shrinkage  of  the  arm  in  a  plethysmograph. 

5.  In  sleep  the  opposite  effects  are  seen :  there  is  a  general  vasodilation 
and  a  fall  in  minimal  blood-pressure  (Howell,  Brush,  and  Fayerweather) . 
There  is  probably  also  a  slight  fall  in  maximal  pressure. 


VARIATIONS  IX  BLOOD-PRESSURE  UNDER  PATHOLOGICAL 

CONDITIONS. 

ASPHYXIA    AND    THE    EFFECT    OF    EXCESS    OF    CO,. 

When  the  heart  fails  the  circulation  is  slowed,  and  the  blood  becomes 
incompletely  aerated  and  overloaded  with  COj  (f.  Bohr).  These  condi- 
tions closely  simulate  the  conditions  present  in  asphyxia  (Traube),  or  after 
breathing  an  atmosphere  overladen  with  COj  (Klug  has  shown  that  the 
effect  of    these   is   quite    similar). 


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Experimental  Asphyxia. — The 

conditions  as  observed  in  experi- 
mental asphyxia  somewhat  fore- 
shadow those  due  to  accumulation 
of  CO,  from  heart  failure.  The 
blood-pressure  changes  in  asphyxia 
have  been  most  carefully  studied 
by  Konow  and  Stcnbeck  in  Tiger- 
stedt's  laboratory,  who  found  as- 
phyxiation in  rabbits  resulting  in 
the  following  series  of  events: 

1.  At  the  beginning  of  asphyxia  the 
vasomotor  and  cardiac  centres 
in  the  medulla  are  stimulated, 
as  is  also  the  inhibitory  centre.  Blood- 
pressure  rises  and  the  pulse  is 
slowed.  (Cameron  has  shown  that,  on 
the  other  hand,  the  tonicity  of  the 
heart  muscle  promptly  decreases 
with  the  first  stage  of  asphyxia  and  re- 
mains diminished  throughout.) 

2.  As  asphyxia  continues,  the  effect 
of  slowing  of  the  pulse  exceeds  that  of 
the  rise  of  pressure  and  the  blood- 
pressure   falls. 

3.  This  condition  slows  the  circula- 
tion still  more,  CO2  accumulates  in  the  blood,  bathing  the  vasomotor  centre,  the  latter 
stimulates  the  arterioles  to  still  further  constriction,  the  vagus  can  no  longer  overcome 
these  effects,  and  in  spite  of  its  continued  action  the  pulse  quickens  and  blood- 
pressureagainrises. 

4.  The  activity  of  the  vasomotor  centre  diminishes  while  the  vagus  centre  remains 
at  maximal  activity,  and  the  pulse-rate  again  slows  and  blood-pres- 
sure  again   falls. 


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Fig.  29. — Diagram  showing  the  curve  of  blood- 
pressure  during  asphyxia.  (Schematic,  illustrating 
the  re.sults  of  Konow  and  Stenbeck.)  A'',  normal; 
BP,  blood-pressure  ;   PR,  pulse-rate. 


28  DISEASES   OF   THE    HEART    AND    AORTA. 

5.  The  vagus  centre  fatigues,  the  accessory  vasomotor  centres  in  the  spinal  cord 
are  again   stimulated,   and   blood -pressure   and    pulse-rate   again    rise. 

6.  Conductivity  of  the  heart  diminishes,  occasional  beats  are  dropped  by  the  ven- 
tricle, blood-pressure  and  pulse -rate  fall,  and  the  animal  dies  at  this 
stage  unless  respiration  is  promptly  restored. 

Occasionally  in  asphyxia  periodic  changes  in  rhythm  of  the  heart  occur,  such  as  have 
been  described  by  Luciani  in  frogs  and  by  Langendorff  in  cats.  These  irregularities  occur 
when  the  vagi  are  sectioned  as  well  as  when  they  are  active;  this  also  occurs  when  the  animal 
is  made  to  breathe  an  excess  of  COj  (Klug).  When,  however,  the  vagi  are  inactive  (cut), 
the  rise  of  blood-pressure  in  asphyxia  is  continuous  from  the  onset  until  the  vasomotor 
centres  fail  (i.e.,  in  the  fourth  stage).  When  the  cervical  nerves  have  been  cut  and  the 
vagi  are  active,  there  is  an  immediate  fall  in  both  blood-pressure  and  pulse-rate;  the  rise 
in  blood-pressure  sets  in  much  later  when  the  accessory  vasomotor  centres  in  the  spinal 
cord  are  stimulated,  or  the  animal  may  die  if  these  fail  to  respond. 

BLOOD-PRESSURE  IN  VARIOUS  DISEASES. 

Importance  of  Determining  the  Mechanism  Producing  the  Change. — 

Variations  in  blood-pressure  occur  not  only  in  conditions  of  health  but  still 
more  under  pathological  conditions.  As  will  be  seen,  the  mechanism  which 
brings  these  changes  about  is  not  always  a  simple  one,  and  the  causal  factor 
may  not  be  affected  by  merely  resorting  to  therapeutic  methods  which 
lower  a  high  blood-pressure  or  raise  a  low  one.  It  is  therefore  necessary 
for  the  clinician  to  investigate  as  far  as  possible  the  condition  of  the  vaso- 
motor nerves,  the  strength  of  the  heart-beat,  to  determine  also  whether  the 
blood  is  properly  aerated,  and  learn  whether  the  kidneys  are  performing 
their  function  properly,  before  proceeding  to  symptomatic  treatment  of 
high  or  low  blood-pressure  when  the  cause  is  in  any  way  obscure. 

DISEASES    WITH    HIGH    BLOOD-PRESSURE    (HYPERTENSION). 

The  following  represent  the  typical  blood-pressure  findings  in  various 
diseases.     In  exceptional  cases  more  extreme  variations  are  seen: 

1.  Nephritis,  especially  the  chronic  forms  (maximal  pressure  160  to  220,  minimal 
120  to  160,  pulse-rate  50  to  80).  High  blood-pressure  is  common  in  both  parenchymatous 
and  interstitial  cases.  Passler  and  Heineke  found  that  in  animals  from  which  almost  all  the 
kidney  substance  had  been  removed,  blood-pressure  rose  pari  passu  with  the  occurrence  of 
signs  of  renal  insufficiency  in  the  metabolism. 

Excellent  reviews  of  this  subject  have  recently  been  published  by 
T.  C.  Janeway  and  by  Pearce.  There  seems  to  be  a  striking  parallelism 
between  continuous  high  blood-pressure  and  oversecretion  of  the  adrenals, 
usually  leading  to  an  hypertrophy  of  the  latter  (see  page  208). 

In  acute  nephritis  the  blood-pressure  may  not  arise,  but  Buttermann  reports 
a  case  of  scarlatinal  nephritis  where  a  rise  of  50  mm.  heralded  the  onset  of  the  nephritis. 
Here  it  is  of  diagnostic  and  prognostic  importance. 

In  uraemia  blood-pressure  rises  at  the  beginning  of  the  attack,  but  may  grad- 
ually fall  a  few  days  before  a  fatal  termination  (Laqueur).  Gradual  fall  in  blood-pressure 
also  accompanies  amelioration.  Engel  finds  that  there  is  no  rise  in  the  mildest  cases  of 
nephritis,  but  that  the  rise  of  pressure  runs  parallel  to  the  severity  of  the  disease  until  the 
terminal  fail  sets  in  from  cardiac  weakness. 

2.  Arteriosclerosis. — Increased  blood-pressure  (maximal  150  to  170,  minimal  110 
to  130,  pulse  60  or  over)  is  the  rule  in  arteriosclerosis,  though  there  are  occasional  excep- 
tions where  the  maximal  pressure  does  not  exceed  or  even  reach  110  mm.  (Israel).  (See 
also  chapter  on  Arteriosclerosis.) 


BLOOD-PRESSURE   AND   BLOOD   VISCOSITY. 


29 


3.  Lead  Poisoning  (plumbism) . — Acute  and  chronic  forms  are  usually  associated  with 
high  blood-pressure,  as  in  arteriosclerosis. 

4.  Chronic  Hypertrophy  of  the  Heart  from  other  causes,  as  in  athletes,  or  as  the 
result  of  smoking  in  excess,  of  compensated  heart  lesions,  etc.  (maximal  pressure  140  to  160, 
minimal  90  to  110  mm.,  pulse-rate  normal  or  increased). 

5.  Aortic  Insufficiency  is  often  but  not  always  associated  with  high  maximal  pres- 
sure (maximal  pressure  170  to  220  mm.  Hg,  minimal  60  to  140,  pulse-rate  usually  increased, 
being  even  as  high  as  120).  This  is  usually  associated  with  arteriosclerosis.    In  young  indi- 


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striped  shading,  pulse-pressure;  dot,  pulse-rate. 


viduals,  as  in  experimental  aortic  insufficiency  in  animals,  the  maximal  pressure  is  usually 
little  changed,  the  minimal  pressure  lowered  (maximal  120  to  130,  minimal  50  to  60,  pulse- 
rate  normal  or  increased). 

6.  Conditions  associated  with  increased  pressure  in  the  cranial  cavity 
(meningitis,  apoplexy,  cerebral  thrombosis,  fracture  of  the 
skull,  intracranial  hemorrhage,  rapidly  growing  brain  tumors, 
some  cases  of  uraemia,  Jacksonian  epilepsy).  Maximal  blood-pressure 
may  rise  to  300  or  400  mm.  Hg,  minimal  pressure  to  160  or  over,  pulse-rate  slow,  60  cr 
under.  Gushing  has  shown  that  when  the  intracranial  pressure  is  raised  above  the  blood- 
pressure,  the  anaemia  of  the  vasomotor  centre  brings  about  a  tremendous  vasoconstriction 
and  action  of  the  augmentor  fibres  in  increasing  the  strength  of  the  heart-beat.  The  blood- 
pressure  rises  in  successive  stages  (Traube-Hering  waves)  until  the  mean  pressure  exceeds 
the  intracranial  pressure.  The  rise  of  blood-pressure  expresses  the 
need   of    the   brain   for  blood;   to  counteract   the  vasoconstriction 


30  DISEASES   OF   THE   HEART   AND    AORTA. 

with  nitrites  or  other  vasoconstrictors  or  by  venesection  only 
increases  the  task  of  the  heart.  The  only  medical  treatment  which  aids  it 
at  all  is  administration  of  atropine  to  paralyze  the  vagi,  quicken  the  heart,  and  permit  the 
pressure  to  rise  more  readily.  Lumbar  puncture  helps  somewhat  by  removing  the  excess  of 
intracranial  fluid.  If  this  does  not  suffice,  Gushing  advises  surgical  interference  in  many 
cases, — a  flap  of  the  skull  being  hfted  temporarily  in  order  to  relieve  the  intracranial  tension 
and  to  allow  the  blood-pressure  to  fall.  This  procedure  is  almost  devoid  of  danger  in  the 
hands  of  a  surgeon  whose  asepsis  is  perfect,  but  very  dangerous  if  it  is  imperfect,  and  this 
point  alone  will  often  decide  the  advisability  or  inadv^sability  of  the  operation. 

7.  Attacks  of  Idiopathic  Epilepsy  are  associated  with  very  high  blood-pressure 
and  slow  pulse.  The  blood-pressure  falls  within  a  few  minutes  after  the  fit,  which  assists  to 
dififerentiate  it  from  uraemia  (Pilcz). 

8.  Vascular  Crises. — Pal  has  described  an  important  group  of  cases  associated  with 
crises  of  high  blood-pressure  due  to  vasoconstriction.  Among  these  he  classes  uraemia, 
certain  cases  of  arteriosclerosis,  especially  with  abdominal  and  cardiac  symptoms,  and 
especially  the  tabetic  visceral  crises  with  intense  pain.  He  has  shown  that  these  as  well  as 
attacks  of  lightning  pains  are  associated  with  marked  vasoconstriction  and  rise  in  blood-pres- 
sure, and  states  that  they  are  even  relieved  by  the  administration  of  nitroglycerin.  He  also 
classes  angina  pectoris,  intermittent  claudication,  and  Raynaud's  disease  under  this  head. 

9.  Attacks  of  Angina  Pectoris. 

10.  Some  Cases  of  Adams^Stokes  Diseases  between  Attacks.  —  Gibson  repor  ts  a 
case  with  maximal  pressure  270,  minimal  pressure  70,  pulse-rate  27.  The  pressure  may, 
however,  never  rise  materially.  During  the  attacks  it  always  falls  almost  to  zero  (see 
page  460). 

11.  Exophthalmic  Goitre  (Graves's  or  Basedow's  disease)  is  often  accompanied  by 
hypertrophy  of  the  heart  with  increased  maximal,  140  to  160  mm.,  minimal  90  to  110 
mm.,  and  pulse-pressure  30  to  50  mm.,  pulse-rat«  accelerated  to  120  and  over.  In 
some  cases  of  Graves's  disease  the  pressure  remains  low  (maximal  120,  minimal  90). 

12.  The  End  of  Pregnancy,  the  onset  of  labor,  and  the  puerperium  are  accom- 
panied by  a  slight  (10-15  mm.)  rise  of  maximal  pressure  with  little  change  in  minimal 
pressure  (Slemons  and  Goldsborough ;  see  Part  III,  Chapter  IX). 

13.  Chronic  Primary  Polycythaemia.  —  The  increased  number  of  red  corpuscles 
increases  the  viscosity  of  the  blood,  and  thereby  the  work  of  the  heart,  besides  arterioscle- 
rosis is  usually  associated.  On  the  other  hand,  as  shown  by  W.  Erb,  Jr.,  increase  in  blood- 
pressure  causes  liquid  to  leave  the  vessels  and  thereby  increases  the  viscosity  of  the  blood 
further — introducing  a  vicious  cycle. 

14.  Cyanosis  in  Heart  Failure  with  Broken  Compensation,  which  occurs  at  some 
stage  in  almost  all  failing  hearts.  The  blood  becomes  overloaded  with  CO^,  and  vasocon- 
striction plus  augmentation  results  as  in  asphyxia  (see  page  237).  Usually  the  pulse  i* 
quickened,  probably  from  fatigue  of  the  vagus  centre.  This  condition  is  of  great  clinical 
importance,  since  the  high  blood-pressure  increases  the  work  of  the  heart  and  accelerates  its 
failure.  Venesection,  nitrites,  digitalis,  anything  which  accelerates  the  velocity  of  blood 
flow  through  the  lungs,  brings  about  improvement  and  lowering  of  the  blood-pressure. 

pathological  conditions  associated  with   low  blood-pressure 

(hypotension). 

Although  the  occurrence  of  low  blood-pressure  is  usually  associated 
in  the  mind  with  the  idea  of  a  diseased  heart,  such  is,  as  a  rule,  not  the 
case.  In  fact,  in  most  chronic  diseases  of  the  heart  the  maximal  pressure 
is  increased  rather  than  decreased,  as  has  been  shown  above.  In  one  case 
of  aortic  insufficiency,  for  example,  the  writer  found  a  maximal  pressure 
of  150  and  a  minimal  pressure  of  110  two  minutes  before  death,  in  spite 
of  intense  heart  failure. 

A  low  blood-pressure  is  more  commonly  an  index  of  fail- 
ure of  the  vasomotor  centre  than  of  the  heart,  and  occurs  in  condi- 
tions where  the  strength  of  the  heart  is  uninjured  (Romberg  and  Passler,  Hasenfeld  and 
Fenevessy,  Crile). 


BLOOD-PRESSURE  AND   BLOOD   VISCOSITY.  31 

Conditions  in  which  low  blood-pressure  is  found  are: 

1.  Acute  infectious  diseases,  except  meningitis  (where  the  blood-pressure  is  high 
from  increased  intracranial  tension).  Romberg  and  Passler  have  shown  that  bacterial 
poisons  diminish  the  tonic  activity  of  the  vasomotor  centre,  and  may  even  paralyze  it. 
The  strength  of  the  heart  is  shown  to  be  undiminished  if  the  vasodilation  is  counteracted  by 
adrenalin,  compression  of  the  abdominal  aorta,  etc.  The  blood-pressure  falls  because  the 
arterioles  are  dilated  and  the  outflow  from  the  arteries  is  too  rapid  (maximal  pressure  90  to 
110,  minimal  pressure  50  to  90,  pulse-rate  increased,  see  table,  page  29). 

The  lowest  blood-pressure  is  in  typhoid  fever  (Barach)  and  peritonitis, 
where  the  dilatation  of  abdominal  vessels  from  the  local  inflammation  add  their  effect  to 
that  of  the  cutaneous  vasodilation.  In  typhoid  fever  the  writer  has  seen  maximal  pressures 
as  low  as  65  mm.  Hg  (Riva-Rocci),  although  maximal  100  to  120  with  minimal  60  to  90  is 
more  common.  Crile  and  Briggs  have  described  rises  in  blood-pressure  at  the  onset  of  per- 
foration due  to  splanchnic  stimulation,  but  the  writer  has  had  two  cases  (one  of  which 
is  mentioned  by  Briggs)  in  which  inactivity  of  the  vasomotor  centre  prevented  this  rise 
from  occurring. 

In  pneumonia  the  blood-pressure  may  not  be  changed  much  (maximal  110  to 
130,  minimal  90,  pulse-rate  120);  it  may  rise  as  mild  asphyxia  sets  in,  or  it  may  fall  very 
low  from  vasomotor  paralysis. 

In  diphtheria,  scarlet  fever,  measles,  acute  rheumatism,  and  • 
and  in  fact  in  all  other  acute  infectious  diseases,  the  maximal  pressure  usually  falls  below 
100  during  the  height  of  the  fever  (Weigert). 

2.  Phthisis.  —  In  this  disease  all  ranges  of  blood-pressure  may  be  found.  John, 
Naumann,  Burckhardt,  and  Stanton  have  found  uniformly  low  pressures,  90  to  100  mm. 
with  the  Gaertner  and  Riva-Rocci  apparatus,  but  this  may  arise  from  the  pallor  of  the  skin. 
Janeway  found  that  variations  of  maximal  pressure  between  80  and  120  mm.  Hg  are 
common  in  the  same  patient,  and  the  writer's  experience  bears  this  out.  The  pulse-rate  is 
usually  rapid,  80  to  100  per  minute.  Peters  finds  that  there  is  usually  a  rise  of  blood-pres- 
sure when  improvement  sets  in,  and  a  fall  when  the  case  is  getting  worse. 

3.  Shock. — Crile  has  shown  that  in  surgical  shock  from  injury  or  pain  there  is  loss 
of  tonic  activity  of  the  vasomotor  centre  exactly  as  in  acute  infectious  diseases.  Syncope 
from  emotional  excitement,  etc.,  is  of  similar  origin.  Crile  counteracts  the  vasomotor 
paralysis  by  putting  a  double-walled  rubber  suit  upon  the  patient  and  inflating  the  cham- 
ber between  the  walls  until  the  pressure  compensates  for  the  loss  of  vascular  tone. 

Henderson,  while  confirming  Crile's  observations  as  regards  the  paresis  of  the  vaso- 
motor centre,  believes  that  this  is  not  the  primary  phenomenon.  He  calls  attention  to  the 
similarity  between  the  phenomena  of  shock  and  those  of  mountain  sickness,  which  Mosso 
has  shown  to  be  due  to  a  low  CO2  content  of  the  blood  (acapnia) ;  Henderson  believes  that 
the  mechanism  of  the  two  conditions  is  similar  and  is  able  to  substantiate  his  claim  by 
producing  shock  experimentally  under  all  conditions  in  which  COj  is  made  to  escape 
rapidly  from  the  blood,  either  through  rapid  aeration  of  the  lungs  or  through  exposure 
of  the  intestines  and  mesentery  to  a  current  of  warm  moist  air.  He  has  shown  further 
that  CO2  is  the  hormone  which  preserves  the  tonic  contraction  of  the  walls  of  the  veins. 
Bancroft  has  also  shown  that  these  are  under  nervous  control  as  well  as  the  arteries  and 
that  their  nerves  arise  in  the  same  regions  as  do  the  vasomotor  nerves  to  the  latter. 

According  to  Henderson  the  sequence  of  events  in  shock  is  as  follows: 

(1)  Pain  or  emotion;  (2)  hyperpnoea;  (3)  overaeration  of  the  blood  (lowering  of  the 
CO2  content,  acapnia),  dilatation  of  the  veins  and  accumulation  of  blood  in  the  latter, 
lowering  of  the  venous  pressure  (and  hence  diminished  entry  of  blood  into  the  heart); 
(4)  fall  in  arterial  pressure,  accompanied  by  loss  of  arterial  tone  (vasodilatation);  (5) 
cerebral  anaemia. 

There  is  an  accumulation  of  blood  in  the  veins  with  depletion  of  the  arteries  (an 
arterial  anaemia). 

In  fevers  the  high  temperature  gives  rise  to  a  slight  polypnoea  and  also  favors 
the  evaporation  of  COj  from  the  lungs.  Henderson  believes  that  these  factors  cooperate 
with  the  toxins  in  producing  the  vasomotor  pareses  of  infectious  diseases. 

It  will  be  seen  that  in  many  of  the  functional  cardiac  diseases  accumulation  of  blood 
in  the  veins  with  depletion  of  the  arteries  is  the  most  striking  disturbance  in  the  circula- 
tion, and  plays  an  important  role  in  producing  the  clinical  picture. 


32  DISEASES   OF   THE   HEART    AND    AORTA. 

Whether  an  occasional  whiff  of  CO2  or  merely  occasionally  holding  the  breath  will 
relieve  the  acapnia  and  restore  the  vascular  tone  in  such  cases  remains  to  be  proved. 

4.  Collapse  from  various  poisons,  carbolic  and  salicylic  acid,  arsenic,  phosphorus, 
drugs  of  the  antipyretic  series,  etc.,  is  due  to  the  same  cause — failure  of  the  vasocon- 
strictor centre, — and  likewise  is  accompanied  by  low  blood-pressure. 

5.  After  extensive  hemorrhage  a  fall  of  blood-pressure  sets  in  (except  after  vene- 
section in  some  cases  where  a  failing  heart  is  relieved),  owing  to  lack  of  blood  to  fill  out 
the  arteries.  This  is  usually  relieved  by  subcutaneous  or  intravenous  NaCl  infusion,  or 
even  by  direct  arterial  transfusion  (Crile). 

6.  In  diarrhoea,  dysentery,  cholera,  or  after  profuse  vomiting,  as  from  cancer 
of  the  stomach,  intestinal  obstruction,  peritonitis,  etc.,  when  large  amounts  of  fluid  have 
left  the  body,  the  arteries  may  also  be  depleted  of  fluid  and  a  very  lov/  blood-pressure 
result.    This  is  also  relieved  by  infusion. 

7.  In  pleurisy,  especially  pleurisy  with  effusion,  blood-pressure  is  uniformly  low. 

8.  Pericarditis  is  accompanied  by  low  blood-pressure  (maximum  100  to  120, 
minimum  70  to  90,  pulse-rate  increased)  unless  complicated  by  hypertrophy  of  the  heart 
or  some  other  factors. 

9.  Acute  cardiac  diseases  of  all  types,  which  have  not  been  preceded  by  chronic 
processes  and  are  not  associated  with  marked  cyanosis.  Here  the  above-mentioned  toxic 
action  on  the  vasomotor  centre  is  usually  present  if  the  endocarditis  is  of  the  infectious 
variety,  and  besides  there  is  some  weakening  of  the  heart.  The  quickened  pulse-rate 
prevents  CO2  from  accumulating  in  the  blood  and  the  asphyxial  rise  in  pressure  does  not 
occur.    K.  Weigert  reports  all  ranges  of  pressure  between  95  and  140  mm.  Hg. 

10.  In  chronic  mitral  stenosis  the  maximal  and  minimal  pressures  are  usually 
normal  or  a  little  below  normal,  when  the  left  ventricle  does  not  hypertrophy;  but  this 
may  vary  considerably. 

11.  Chronic  wasting  diseases,  cancer,  chronic  phthisis,  anaemias,  etc.,  are  associated 
with  brown  atrophy  of  the  heart  muscle  (see  page  211),  with  weakened  heart  action, 
hence  with  lowered  blood-pressure  (10  to  20  mm.  lower  than  normal,  pulse-rate  usually 
increased). 

BLOOD-PRESSURE   IN   THE   VEINS. 

Various  methods  have  been  devised  for  the  determination  of  the  venous 
blood-pressure  in  man,  the  first  being  introduced  by  v.  Basch  and  being 
but  a  sHght  variation  of  his  arterial  sphygmomanometer. 

A  very  similar  apparatus  has  been  constructed  recently  by  Sewall,  but  this  gives 
rather  unsatisfactory  results  in  practice.  V.  Frey  and  later  Gaertner  also  determined 
the  pressure  by  considering  it  equal  to  the  height  above  the  angle  of  Ludwig  at  which 
the  veins  of  the  hand  could  be  seen  to  collapse.  This  method  is  not  quite  as  good  as  the 
former.  A  considerable  advance  was  made  by  v.  Recklinghausen,  who  compressed  the 
vein  by  inflating  a  small  rubber  capsule  provided  with  a  glass  window  in  the  top  and  a 
rubber-dam  floor  having  a  hole  in  its  centre.  This  dam  was  coated  with  glycerin  so  as  to 
insure  perfect  contact.  It  is  then  placed  over  a  vein,  preferably  upon  the  back  of  the  hand 
or  wrist,  and  the  system  blown  up  until  the  vein  can  be  seen  to  disappear,  at  which  point 
the  pressure  is  read  off  upon  a  water  manometer.  Eyster  and  Hooker  have  modified  this 
chamber  by  constructing  one  of  aluminum  with  the  entire  top  of  glass  and  the  two  ends 
concave  so  as  to  avoid  pressure  upon  the  veins,  and  their  apparatus  seems  to  give  results 
concordant  within  1  cm.  HjO.  They  find  that  the  normal  venous  pressure  at  the  sterno- 
xiphoid  articulation  is  5-10  cm.  HjO.'  It  is  increased  by  exercise  and  in  cardiac  cases 
with  broken  compensation,  when  it  may  rise  to  27  cm.  or  over.  When  the  veins  are  not 
sufficiently  distended  at  that  level  the  hand  may  be  lowered  a  known  distance,  the 
pressure  read;  and  the  distance  lowered  subtracted  from  the  amount  of  the  reading  will 
represent  the  venous  pressure.  In  cases  where  phlebosclerosis  is  present  no  satisfactory 
determinations  could  be  made. 

'  These  figures  agree  well  with  direct  manometric  determinations  recently  made  in 
man  by  Moritz  and  v.  Tabora  (Verhandl.  d.  Kong.  f.  innere  Med.,  1909,  xxvi,  378). 


BLOOD-PRESSURE   AND    BLOOD   VISCOSITY. 


33 


The  pressure  in  the  capillaries  of  vascular  areas,  especially  of  the 
be  determined  in  the  same  way,  using  the  point  of  blanching  as  the 

The  study  of  the  venous  pres- 
sure is  of  undoubted  importance 
as  an  index  of  accumulation  of 
the  blood  in  the  systemic  circu- 
lation and  thus  as  an  index  of 
heart  failure.  Moreover,  it  is  the 
most  important  physiological 
factor  bringing  about  variations 
in  the  volume  of  the  heart;  a  high 
venous  pressure  causing  dilata- 
tion, alow  venous  pressure  causing 
diminution  in  volume  (insufficient 
filling) .  This  may  prove  to  be  an 
important  factor  in  bringing  about 
certain  conditions  in  which  there 
is  "arterial  anaemia"  (shock,  car- 
diac neurosis,  etc.) . 


THE  PULMONARY  CIRCULATION- 


lips,  may 
criterion. 


Before  birth  the  resistance  in 
the  vessels  of  the  collapsed  lung  is 
greater  than  that  in  the  systemic 
arteries,  and  hence  blood  passes 
from  the  pulmonary  artery  to 
the  aorta  through  the  ductus 
arteriosus  (Botalli). 


Fig.  31. — Hooker  and  Eyster's  modification  of 
V.  Recklinghausen's  method  of  determining  the  venous 
pressure  in  man. 


As  the  blood -pressure  in  young 
infants  is  80  mm.  Hg  (Trumpp),  it  must 
be  assumed  that  the  pulmonary  pressure 

is  somewhat  greater  than  this.  When  the  area  of  lung  capillaries  widens  with  the  first 
inspiration,  the  resistance  in  the  pulmonary  vessels  decreases  very  markedly.  This 
decrease  continues  during  the  period  of  infancy  until  the  lung  is  fully  expanded. 
According  to  a  number  of  observers  (Beutner,  Lichtheim,  Openchowski,  Bradford  and 
Dean,  Plumier),  the  mean  pressure  in  the  pulmonary  artery  of  rabbits,  cats,  and  dogs 
varies  from  6  to  35  mm.  Hg.  It  may  be  said  to  be  approximately  one-third 
that  of  the  aorta  but  subject  to  considerable  variations.  Tigerstedt  has  found 
that  in  rabbits  with  142  mm.  pressure  in  the  aorta  the  pressure  within  the  right  ventricle 
is  much  greater  than  this. 

The  pulse-pressure  in  the  pulmonary  artery  is  much  smaller  than  that 
in  the  aorta,  probably  about  6-12.5  mm.  Hg  in  small  animals,  and  in 
man  not  far  from  these  figures. 

Work  of  the  Right  Heart. — The  pressure  within  the  pulmonary  artery 
and  hence  the  work  of  the  right  heart  varies  within  wide  limits  under 
experimental  conditions. 

These  variations  are  in  part  passive,  due  to  passive  stasis  of  blood 
within  the  pulmonary  vessels,  and  in  part  may  be  the  result  of  vaso- 
motor changes  in  the  pulmonary  vessels. 
3 


34  DISEASES   OF   THE   HEART    AND    AORTA. 

The  conditions  in  which  the  changes  in  pulmonary  pressure  arise 
passively  from  changes  in  the  left  ventricle  are  the  most  common  and  are 
clinically^  the  most  important. 

Increased  mean  pulmonary  pressure  may  arise: 

1.  When  an  increased  amount  of  blood  enters  the  right  heart  from  the  veins  and  is 
expelled  into  the  pulmonary  artery. 

2.  The  pulmonary  blood-pressure  also  undergoes  rhythmic  variations,  falling  during 
inspiration  as  a  result  of  suction  (as  shown  by  de  Jager)  and  rising  during  expiration. 

3.  When  the  left  ventricle  fails  to  pump  an  equal  amount  onward  into  the  aorta, 
causing  blood  to  accumulate  in  the  pulmonary  capillaries  until  these  are  overfilled  and 
aid  in  increasing  the  resistance  in  this  circuit.  (The  left  ventricle  acts  upon  the  pul- 
monary circulation  as  a  suction  pump.) 

4.  Probably  from  constriction  of  the  pulmonary  arteries  under  the  influence  of 
vasomotor  nerves. 

Pulmonary  Vasomotor  Nerves. — The  existence  of  vasomotor  nerves  in 
the  pulmonary  artery,  first  suggested  by  Brown-Sequard  (1870  to  1873)  and 
later  by  Badoud,  has  been  much  disputed,  but  seems  now  to  be  proved. 

Fran?ois-Franck  has  shown  that  stimulation  of  the  lower  cervical  and  upper  five 
thoracic  ganglia  in  the  dog  uniformly  caused  a  rise  of  blood-pressure  in  the  pulmonary 
artery,  a  fall  of  pressure  in  the  left  auricle,  and  an  increase  in  the  volume  of  the  lungs, 
probably  due  to  accumulation  of  blood  on  the  arterial  side  of  the  capillaries.  This  rise  in 
pulmonary  pressure  bore  no  constant  relation  to  the  pressure  in  the  femoral  artery,  which 
sometimes  rose  and  sometimes  fell.  This  evidence  strongly  favors  the  existence  of  vasocon- 
strictor fibres.  Fran^ois-Franck  showed  further  that  these  same  changes  in  pulmonary 
arterial  pressure,  left  auricular  pressure,  and  lung  volume  occurred  reflexly  when  the  central 
end  of  the  femoral  nerve  or  a  proximal  branch  of  the  solar  plexus  was  stimulated.  This 
reflex,  as  he  shows  in  a  subsequent  paper,  may  have  important  bearings  in  the  production 
of  certain  cardiac  symptoms  and  in  influencing  the  course  of  cardiac  diseases. 

Action  of  Drugs  on  the  Pulmonary  Circulation. — Frangois-Franck's  re- 
searches are  very  convincing.  They  have  been  confirmed  by  H.  C.  Wood,  Jr., 
and  others,  and  are  accepted  by  as  keen  a  critic  as  Tigerstedt;  but  Wood,  Jr., 
and  also  Petitjean  have  found  that  all  drugs  exert  a  much  less 
marked  effect  on  the  pulmonary  circulation  than  on  the 
systemic.  It  must  be  admitted  that  acceptance  is  not  universal.  The 
clinical  importance  of  the  problem  renders  it  a  matter  of  universal  interest. 

It  may  be  considered  proved  by  Frangois-Franck's  work  that  sensory 
stimuli,  stimulation  of  the  sympathetic  nerves,  asphyxia,  etc.,  may  cause 
the  pulmonary  arterial  pressure  to  rise  to  about  double  its  original  height, 
and  hence  in  chronic  conditions  may  play  an  important  ratio  in  bringing 
about  hypertrophy  of  the  right  ventricle.  Moreover,  changes  of  pressure 
which  are  relatively  small  when  applied  to  the  left  ventricle  assume  much 
greater  proportions  when  applied  to  the  weaker  right  ventricle,  and  appar- 
ently slight  changes  in  the  strength  of  this  chamber  may  then  be  impor- 
tant factors  in  the  mechanism  of  the  circulation. 

Tonicity  of  the  Right  Ventricle. — More  important  than  the  changes  in 
pressure  in  the  pulmonary  artery  are  the  changes  in  tonus  of  the  right 
ventricle.  Owing  to  the  thinness  of  the  wall,  changes  in  tonicity  affect 
this  chamber  much  more  readily  than  they  do  the  left;  overstretching  of 
the  fibres  sets  in  more  readily,  and  weakening  of  the  right  ventricle  results 
more  readily.  These  changes  may  have  no  direct  relation  to  the  changes 
in  pulmonary  arterial  pressure. 


BLOOD-PRESSURE   AND   BLOOD   VISCOSITY.  35 

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36  DISEASES   OF  THE   HEART    AND    AORTA. 

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Bowen,  W.  P.:  Study  of  the  Pulse-rate  in  Man  as  Modified  by  Muscular  "Work,  Contrib. 
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Howell,  W.  H.:  A  Contribution  to  the  Physiology  of  Sleep,  Jour.  Exper.  Med.,  N.  York, 
1897,  ii,  313. 

Brush,  C.  E.,  and  Fayerweather,  R.:  Observations  on  the  Changes  in  Blood-pressure 
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Bohr,  Chr.:  Physiologic  der  Atmung,  W.  Nagel's  Handb.  d.  Physiol,  d.  Menschen,  Braun- 
schweig, 1906,  Bd.  i. 

Traube,  L.:  Von  den  Erscheinungen,  Welche  man  am  Circulations  apparat.  bei  Einblasung 
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stoff  und  Stickstoff  beobachtet,  Ges.  Beitrage  zur  Pathol,  u.  Physiol.,  Berl.,  1878, 
i,  332. 

Klug,  F.:  Ueber  den  Einfluss  der  Kohlensaure  und  des  Sauerstoffs  auf  die  Function  des 
Saugethierherzens,  Arch.  f.  Physiol.,  Leipz.,  1883,  p.  134. 

Konow,  H.  G.,  and  Stenbeck,  Th.  :  Ueber  die  Erscheinungen  des  Blutdruckes  bei  Erstick- 

vmg,  Skand.  Arch.  f.  Physiol.,  Leipz.,  1889,  i,  403. 
^Langendorff,    O.;    Untersuchungen    ueber    die    Natur    die    des    periodisch-aussetzenden 
Rhythmus  insbesondere  des  Herzens,  Arch.  f.  d.  ges.  Physiol.,  Bonn,  1907,  cxxi,  54. 

Passler,  H.:  Ueber  die  Ursache  und  Bedeutung  der  Herzaffektion  Nierenkranker,  Samml. 
kUn.  Vortrage,  Leipz.,  1906,  Inn.  Med.,  No.  123. 

Buttermann:  Einige  Beobachtungen  ueber  den  verhalten  des  Blutdruckes  bei  Kranken., 
Deutsch.  Arch.  f.  klin.  Med.,  Leipz.,  1902,  Ixxiv,  1. 

Janeway,  T.  C:  The  Pathological  Physiology  of  Chronic  Arterial  Hypertension  and  its 
Treatment,  Am.  Jour.  M.  Sc.,  Phila.,  1907,  cxxxiii,  50. 

Pearce,  R.  M.:  The  Theory  of  Chemical  Correlation  as  Applied  to  the  Pathology  of  the 
Kidney,  Arch.  Int.  Med.,  Chicago,  1908,  ii,  77. 

Laqueur,  A.:  Zur  Kenntniss  uraemischer  Zustande,  Deutsch.  med.  Wochnschr.,  Leipz., 
1901,  xxAai,  744. 

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d.  deutsch.  Naturforsch.  u.  Aerzte;  Zentralb.  f.  d.  ges.  Phvsiol.  u.  Path.  d.  Stoffw., 
Berl.,  1908,  iii,  832. 

Israel,  A.:  Klinische  Beobachtimgen  ueber  das  Symptom  der  Hypertension,  Samml.  klin. 
Vortrage,  Leipz.,  1907;   Inn.  Med.  No.  135,  136;   and  In.  Diss.,  Strasburg,  1907. 

dishing,  H.  W.:  Some  Experimental  and  Clinical  Observations  Concerning  States  of 
Increased  Intracranial  Tension,  Am.  Jour.  M.  Sc,  Phila.,  1902,  cxxiv,  375.  The  Blood- 
pressure  Reaction  of  Acute  Cerebral  Compression  Illustrated  by  Cases  of  Acute  Cerebral 
Hemorrhage,  ibid.,  1903,  cxxv,  1017. 

Hill,  L.:  The  Mechanism  of  the  Circulation,  Schafer's  Text-book  of  Physiol.,  Edinb.  and 
Lond.,  1900,  ii,  1.    The  Cerebral  Circulation,  Lond.,  1896. 

Kocher,  Th.:  Himerschutterung,  Himdruck,  u.  s.  w.  Nothnagel's  Handb.  d.  spec.  Pathol, 
u.  Therap.,  Wien,  1901,  vol.  ix,  iiiter  Theil,  iite  Abtheilung. 

Pilcz,  A.:  Ueber  einige  Ergebnisse  von  Blutdruckmessungen  bei  Geisteskranken,  Wien. 
klin.  Wochenschr.,  Wien,  1900,  xiii,  276. 

Pal,  J.:  Die  Gefasskrisen,  Leipz.,  1905. 


BLOOD-PRESSURE   AND   BLOOD   VISCOSITY.  37 

Gibson,  G.  A.:  Heart-block,  Brit.  M.  J.,  Lond.,  1906,  ii,  1113. 

Slemons,  J.  M.,  and  Goldsborough,  F.  C.     See  chapter  on  Pregnancy. 

Hasenfeld,   A.,  and  Fenevessy,   B.:  Ueber  die  Leistungsfahigkeit  des  fettig   entarteten 

Herzens,  Berl.  klin.  Wchnschr.,  1899,  xxxvi,  80,  125,  150. 
Crile,  G.:  The  Blood-pressure  in  Surgery,  Phila.,  1903. 
Henderson,  Y.  (with  the  collaboration  of  M.  McR.  Scarborough,  F.  P.  Chillingworth,  and 

J.  R.  Coffey):  Acapnia  and  Shock.    I,  Carbon  Dioxide  as  a  Factor  in  the  Regulation 

of  the  Heart-rate,  Am.  Journ.  Physiol.,  Bost.,  1908,  xxi,  126;   Part  II,  ibid.,  1909, 

xxiii,  345,  and  Part  III,  ibid.,  1909,  xxiv,  66. 
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1878,  Fisiologia  dell'uomo  suUa  Alpi,  2d  ed.,  1888. 
Mosso,   A.:  La    respiration    periodique   (phenomene   de   Cheyne-Stokes)  telle   qu'elle   se 

produit  chez  I'homme  sur  les  Alpes  par  I'effet  de  I'acapnie,  Arch.  ital.  de  biol.,  Turin, 

1905,  xliii,  81.     Differences  individuelles  dans  la  resistance  a  la  pression  partie  le  de 

I'oxygene,  ibid.,   1905,  Ixiii,   197.     Demonstration  des  centres  respiratoires  spinaux 

au  moyen  de  I'acapnie,  ibid.,  1905,  Ixiii,  216. 
Barach,  J.  H.:  Blood-pressure  Studies  in  Typhoid,  N.  York  M.  J.,  1907,  Ixxvi,  348. 
Crile,  G.:  Diagnostic  Value  of  Blood-pressure  Determinations  in  the  Diagnosis  of  Typhoid 

Perforation,  Jour.  Am.  M.  Assoc.,  Chicago,  1903,  xl,  1292. 
Briggs,  J.  W.,  and  Cook,  H.  W.:  Clinical  Observations  on  Blood-pressure,  Johns  Hopkins 

Hosp.  Bull.,  Bait.,  1903,  xi,  451. 
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krankheiten,  Samml.  kUn.  Vortrage,  Leipz.,  1907,  Inn.  Med.,  No.  138. 
John,  M.:  Ueber  den  arteriellen  Blutdruck  bei  Phthisiker,  Ztschr.  f.  diat.  u.  physik.  Therap., 

Leipz.,  1901,  V,  275. 
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tenw.,  Leipz.,  1904,  v,  118. 
Stanton,  W.  B.:  The  Blood-pressure  in  Tuberculosis,  Internat.  Clin.,  Phila.,  1907,  17th 

Ser.,  60. 
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Med.,  Chicago,  1908,  ii,  42. 
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Chicago,  1906,'xlvii,  189. 
V.  Recklinghausen,  H.:  Unblutige  Blutdruckmessung,  Arch.  f.  exper.  Path.  u.  Pharmakol., 

Leipz.,  1906,  Iv. 
Hooker,  D.  R.,  and  Eyster,  J.  A.  E.:  An  Instrument  for  the  Determination  of  Venous  Pres- 
sure in  Man,  Johns  Hopkins  Hosp.  Bull.,  Bait.,  1908,  xix,  274. 

Pulmonary  Circul.\tion. 

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heilk.,  Berl.,  1906,  Ixiii,  43. 
Beutner,  Lichtheim,  Openchowski,  Bradford  and  Dean,  Plumier,  quoted  from  Tigerstedt, 

R.:  Der  kleine  Kreislauf,  Ergeb.  d.  Physiologic,  Wiesb.,  1903,  ii,  528  (in  which  a  com- 
plete summary  of  the  literature  to  that  date  is  to  be  found,  with  an  excellent  resume 

of  the  facts). 
De  Jager,  S.:  Ueber  den  Blutstrom  in  den  Lungen,  Arch.  f.  d.  ges.  Physiol.,  Bonn,  1879, 

xxi,  426. 
Franyois-Franck,  Ch.  A.:  Nouvelles  recherches  sur  Taction  vaso-constrictive  pulmonaire 

du  grand  sympathique,  Arch,  de  physiol.  nor.  et  path.,  Par.,  1895,  5  Ser.,  vii,  744,  816. 

Etude  critique  et  experimentale  de  la  vasoconstriction  pulmonafre  reflexe,  ibid.,  1896, 

5  Ser.,  viii,  178,  193. 
Wood,  H.  C,  Jr.:  A  Physiological  Study  of  the  Pulmonary  Circulation,  Am.  Jour.  Physiol., 

Bost.,  1902,  vi,  283. 
Petitjean,  G.:  Action  de  quelques  medicaments  vasomoteurs  (nitrite  d'amyle,  adrenaline, 

ergot  de  seigle)  sur  la  circulation  pulmonaire,  J.  de  physiol.  et  de  path,  gen.,  Par., 

1908,  X,  403. 


38 


DISEASES   OF   THE   HEART    AND    AORTA. 


VISCOSITY  OF  THE  BLOOD. 

One  of  the  most  important  factors  in  determining  the  work  of  the  heart 
and  the  nutriment  of  the  tissues  is  the  viscosity  of  the  blood, — that  is,  the 
friction  which  its  molecules  exert  upon  each  other  and  upon  the  walls  of 
the  blood-vessels. 

Poisseuille  and  later  Arrhenius  introduced  a  method  for  determining  viscosity  quan- 
titatively for  indifferent  fluids  by  observing  the  time  taken  for  a  given  volume  of  fluid  to 
flow  vertically  down  a  given  length  of  capillary  tube.  The  time  taken  by  water  to  flow 
under  the  same  conditions  was  used  as  the  unit.    Poisseuille  found 

Quantity  of  blood  flowing  in  given  time  =  viscosity  coefficient  X  (diameter  of 
capillary)^  X  height  of  pressure  :  length  of  tube  for  distance  of  flow. 

Huerthle  found  that  Poisseuille's  law  also  held  for  pulsating  fluids  and  measured  the 
viscosity  of  the  blood  in  the  living  animal  by  comparing  the  outflow  of  blood  from  a  capil- 
lary tube  introduced  into  the  aorta  to  the  outflow  of  water  under  the  same  conditions. 

Viscosity  coefficient  (water)  =  4700 
Dog's  blood  =  1045 

Water  4700      .  .     ^     ^  . 

Coefficient  of  viscosity. 


Dog's  blood       1045 


=  4.5 


Apparatus  for  Clinical  Determination  of  Viscosity. — Various  forms  of 

apparatus  have  been  devised  for  determining  the  viscosity  clinically,  most 

of  them  depending  upon  the  time  taken  for  a  column  of  blood  in  a  given 

^  capillary  to  traverse  a  given  distance 

or  to  flow  out  of  a  given  orifice  when 

subjected  to  the  pressure  exerted  by 

a  constant  column  of  water. 

WATERJACKET 


Fig.  32. — Determann's  apparatus  for  determining  the  viscosity  of  the  blood.  (After  Brugsch  and 
Schittenhelm.)  A.  Apparatus  at  rest  on  its  stand,  pivoted  on  the  thermometer  and  the  handle  as  an  axis. 
In  the  blood-receiving  tube  within  the  ■water-jacket  ae=df,  ab  =  cd.  B.  Method  of  application.  (After 
Brugsch  and  Schittenhelm.) 


Such  apparatus  has  been  described  by  Huerthle,  Burton-Opitz,  Hirsch  and  Beck, 
Determann,  Hess  and  also  McCaskey  have  devised  very  simple  forms  of  apparatus  in 
which  suction  from  a  rubber  bulb  is  used  instead  of  positive  pressure.  C.  R.  Austrian  in  the 
Johns  Hopkins  Medical  Clinic  has  found  that  the  Hess  apparatus  gives  results  with  normal 
blood  which  tally  well  with  the  blood  count,  and  which  therefore  seem  quite  satisfactory. 

Determann's  newer  apparatus  (Fig.  32),  however,  combines  clinical 
convenience  with  accuracy  and  is  probably  the  most  satisfactory  now  in  use.  It  con- 
sists of  a  capillary  tube  surrounded  by  a  small  condenser-jacket  of  glass  containing  water 
at  38°.    The  jacket  bears  two  side  arms  which  rest  in  the  forks  of  two  uprights  so  that  the 


BLOOD-PRESSURE  AND   BLOOD   VISCOSITY.  39 

jackets  always  assume  a  vertical  position.  The  apparatus  is  taken  up  as  a  whole  and  the 
blood  sucked  up  to  a  mark  on  the  capillary.  The  apparatus  is  then  placed  back  on  the 
forks,  and  the  time  taken  for  the  blood  to  flow  out  until  it  reaches  a  second  (lower)  mark 
is  noted.  (This  should  require  30-40  seconds.)  A  similar  determination  is  made  with  water 
(6-8  seconds). 

In  order  to  keep  the  blood  from  clotting,  a  little  hirudin  may  be  placed  upon  the 
ear  before  stabbing  it.  This  does  not  alter  the  viscosity  as  do  adding  sodium  oxalate, 
laking,  and  defibrination;  and  keeps  the  blood  from  clotting  for  20-30  minutes. 

Determann  obtains  a  few  drops  of  blood  quickly  by  having  the  patient  exert  a  forced 
expiration  with  the  glottis  closed  (Valsalva's  experiment). 

Factors  Influencing  Viscosity. — Heubner,  Determann,  and  others  have 
found  that  the  chief  factor  in  determining  the  viscosity  is  the  viscosity  of 
the  red  corpuscles,  to  which  about  two-thirds  of  the  viscosity  of  the  blood  is 
due.  Indeed  in  many  cases  these  observers,  and  also  Austrian,  have  found 
that  the  blood-count  and  the  viscosity  furnish  accurate  controls  of  one 
another, —  though  there  are  exceptions  under  pathological  conditions 
(leukaemia,  etc.).  There  is  little  if  an}'^  difference  between  the  viscosity  of 
the  normal  blood  in  the  arteries,  capillaries,  and  veins.  But  in  venous 
stasis  the  viscosity  increases  tremendously. 

In  a  polycythaemica  with  11,000,000  red  corpuscles  the  vis- 
cosity may    be  three    or    more    times   the    normal    (Stern). 

On  the  other  hand,  in  anaemias,  fever,  the  hydraemia 
which  is  associated  with  anasarca  in  broken  compensation  or  exudates  the 
viscosity  is  uniformly  greatly  diminished. 

Burton-Opitz  found  that  diet  exerted  a  considerable  effect,  meat 
raising  the  viscosity,  carbohydrates  and  fats  lowering  it. 
He  also  found  that  hot  baths  lowered  viscosity  while  cold  baths  increased 
it.     Hot-air  baths  seem  to  have  little  effect. 

In  compensated  heart  disease  the  water  content  of  the  blood  does  not 
change  (Askanazy),  nor  does  the  viscosity,  but  the  water  is  increased  and 
the  viscosity  diminished  (3.74  to  4.21)  when  compensation  is  broken  (Deter- 
mann).   In  bronchitis  and  diabetes  it  is  high  (5.5). 

Determann  cannot  confirm  the  findings  of  Otfried  MlUler  and  Inada 
that  potassium  iodide  lowers  viscosity;  and  indeed  the  changes  which  they 
obtained  were  less  than  1.0  per  cent.,  well  within  the  limits  of  experimental 
error.  Their  paper,  as  well  as  those  of  Hirsch  and  Beck,  illustrates  the 
tendency  of  workers  in  the  field  to  draw  too  definite  conclusions  from  too 
small  variations. 

BIBLIOGRAPHY. 

Viscosity. 

Poisseuille:  An  de  chim.  et  de  phys..  Par.,  1847,  3  s6r.,  i,  21  (quoted  from  Hirsch  and  Beck). 

Arrhenius,  S.:  Innere  Reibung  wasseriger  Losungen,  Ztschr.  f.  physik.  Chem.,  Leipz.,  1887, 
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Huerthle,  K.:  Widerstand  der  Blutbahn,  Deutsch.  med.  Wochenschr.,  Leipz.,  1897,  809. 
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Ergebnisse,  Arch.  f.  d.  ges.  Physiol.,  Bonn,  1900,  Ixxxii,  415. 

Burton-Opitz,  R.:  Ueber  die  Veranderung  der  Viskositat  des  Blutes  unter  dem  Einfluss 
verschiedenes  Ernahrung  und  experimenteller  Eingriffe,  Arch.  f.  d.  ges.  Physiol., 
Bonn,  1900,  Ixxxii,  447.  Vergleich  der  Viskositat  des  normalen  mit  der  des  Oxalat- 
blutes  und  des  defibrinirten  Blutes  und  des  Blutserums  bei  verschiedener  Tempera- 
ture, ibid.,  1900,  Ixxxii,  464.    Weitere  studien  ueber  die  Viskositat  des  Blutes,  ibid., 


40  DISEASES   OF   THE   HEART   AND   AORTA. 

1906,  cxii,  189;   also  Am.  Med.,  1900,  vii,  111.    The  Effect  of  Changes  in  Tempera- 
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The  Effect  of  Intravenous  Injections  of  Solutions  of  Dextrose  upon  the  Viscosity  of 

the  Blood,  ibid.,  viii,  240. 
Hirsch,  C,  and  Beck,  C:  Studien  zur  Lehre  von  der  Viscositat  (innere   Reibung)  des 

lebenden  menschlichen  Blutes,  Deutsch.  Arch.  f.  klin.  Med.,  Leipz.,  1900,  Ixix,  503; 

and  1902,  Ixxii,  560. 
Detemiann:  Klinische  Untersuchungen  ueber  die  Viskositat  des  menschlichen  Blutes, 

Ztschr.  f.  klin.  Med.,  Berl.,  1906,  lix,  283.    Discussion  upon  this  paper  in  the  Zentralbl. 

f.  inn.  Med.,  1906,  xxvii,  519.     Die  Beinflussung  der  Viskositat  des  menschlichen 

Blutes  durch  Kaltereize  Warmeentziehung,  Warmezufuhr,  und  Warmestauung,  Berl. 

klin.  Wochnschr.,  1907,  xUv,  687,  723. 
Hess,  W.:  Ein  neuer  Apparat  zur  Bestimmung  der  Viscositat  des  Blutes,  Cor.-Bl.  f.  schweiz 

Aerzte,  Basel,  1907,  xxxvii,  73. 
McCaskey,  G.  W.:  The  Viscosity  of  the  Blood;   Its  Value  in  Clinical  Medicine,  J.  Am.  M. 

Assoc.,  Chicago,  1908,  li,  1653. 
Determann:  Ein    einfaches,    stets    gebrauchfertiges    Blutviskosimeter,    Muenchen    ined. 

Wochnschr.,  1907,  liv,  1130. 
Heubner,  W.:  Die  Viskositat  des  Blutes,  Arch.  f.  exper.  Pathol  u.  Pharmakol.,  Leipz., 

1905,  liii,  280. 
Stem:  Discussion  of  Determann's  paper. 
Askanasy,  S.:  Ueber  den  Wassergehalt  des  Blutes  und  des  Blutserums  bei  Kreislaufstorung, 

ii.  s.  w.,  Deutsch.  Arch.  f.  klin.  Med.,  Leipz.,  1897,  lix,  385. 


III. 

THE    ARTERIAL    PULSE. 

Historical. — Observation  of  the  arterial  pulse  began  almost  synchronously  with  the 
accurate  observation  of  disease  in  general.  Hippocrates  (B.  C.  500)  noted  the  marked 
pulsation  (a^nj/zof)  of  the  arteries  in  certain  diseases,  but  did  not  associate  it  with  the  beat 
of  the  heart.  Herophilus  (B.  C.  300)  observed  the  relative  synchronism  of  these  two  events 
and  speaks  of  the  quiet  pulse  in  health  (pfvyfioq)  in  contrast  to  the  marked  pulsation  in 
disease  (the  naliio^  of  Hippocrates).  Eristratus  (B.  C.  280)  showed  that  the  arteries  near 
the  heart  beat  before  the  arteries  more  distant  from  it.  Aristotle  and  later  Archigenes 
(first  century  after  the  Christian  era)  made  numerous  observations  upon  the  pulse  in  various 
diseases,  and  the  latter  described  and  gave  the  name  to  the  dicrotic  type  in  cases 
of  fever,  although  he  still  believed  that  the  arteries  were  filled  with  air.  Galen  (A.  D.  131 
202)  demonstrated  that  the  arteries  were  filled  with  blood  and  studied  the  influence  of  sex, 
age,  climate,  sleep,  hot  and  cold  baths  upon  the  rhythm  of  the  pulse. 

The  old  Chinese  physicians  also  described  the  pulse  and  even  made  drawings  to 
illustrate  their  sensory  impressions — a  practice  which  did  not  begin  in  Europe  until  the 
time  of  Henri  Fouquet  in  1767.  After  Harvey's  demonstration  of  the  circulation  of  the 
blood  (1628),  the  study  of  the  pulse  was  resumed  with  renewed  vigor  and  has  continued 
to  the  present  day. 

Examination  of  the  Pulse. — The  characteristics  of  the  pulse-wave  are, 
as  a  rule,  determined  upon  the  radial  artery,  in  which  the  arterial  tension 
may  be  estimated  as  described  on  page  19,  the  wall  of  the  artery  being  also 
rolled  under  the  finger  while  the  artery  is  empty,  and  thus  the  presence  or 
absence  of  arteriosclerosis  noted.  The  walls  of  a  normal  artery  are  barely, 
if  at  all,  palpable;  an  atheromatous  artery  may  feel  like  the  trachea  of  a 
small  animal  (goose-neck);  a  diffusely  sclerotic  artery  feels  like  a  piece  of 
thick-walled  rubber  tube. 

It  is  important  to  note  the  palpability  of  several  arteries,  since  one 
of  them  may  escape  a  sclerotic  process.  All  the  blood  must  have  been 
pressed  out  of  their  lumina  and  of  the  vense  comites  that  accompany  them 
before  palpation  is  begun,  or  else  normal  arteries  may  appear  to  be 
sclerotic.  The  pressure  is  then  relieved,  and  the  tips  of  two  or  three  fingers 
are  pressed  upon  the  artery  until  the  pulse  appears  maximal  (at  about 
the  minimal  pressure),  when  the  following  characteristics  are  noted:  (1) 
whether  the  artery  (hence  the  pulse)  feels  large  and  dilated  (pulsus  mag- 
nus)  or  small  and  constricted  (pulsus  parvus);  (2)  whether  the 
pulse  is  hard  (pulsus  d u r u s)  or  soft  (pulsus  molli s) ,— i.e.,  whether 
the  minimal  pressure  is  low  or  high;  (3)  whether  the  onset  of  the  wave  is 
sudden  (pulsus  celer)or  gradual  ( p  u  Is  u  s  tardus);  (4)  whether 
the  wave  is  sustained  (anacrotic)  or  subsides  suddenly  under  the 
finger  (collapsing,  water-hammer,  or  Corrigan  pulse) ;  (5)  the 
rate  of  the  heart  per  minute  (counted  continuously  during  at  least  a  half 
minute) ;  (6)  whether  the  rhythm  is  regular  (pulsus  rcgularis)Gr 
irregular   (pulsus    irregularis). 

Clinical  Sphygmographs.  —  An  instrument  (sphygmograph)  to 
record  the  pulse-wave  graphically  was  first  devised  by  K.  Vierordt  (1855), 

41 


42 


DISEASES   OF   THE    HEART    AND    AORTA. 


but  it  was  not  until  1860  that  E.  J.  Marey  devised  a  thoroughly  practi- 
cal and  accurate  form,  almost  devoid  of  error,  which  is  still  in  use. 

Marey's  sphygmograph  consists  of  a  button  (pelotte)  pressed  against  the  skin  over 
the  artery  by  means  of  a  spring  so  as  to  receive  the  pulsations  from  the  artery.  It  is  held 
in  place  by  a  leather  cuff,  and  it  is  most  important  that  the  pelotte  remain  exactly  over  and 
not  to  one  side  of  the  artery.  The  pelotte  is  surmounted  by  a  vertical  rod  or  screw  which 
articulates  by  a  movable  joint  with  a  long  writing  lever.  The  writing  lever  records  the 
magnified  pulse  movements  upon  a  surface  of  smoked  paper  held  in  vertical  position  by  a 
brass  upright  and  driven  by  a  small  piece  of  clock-work. 

A  more  compact  and  convenient  form  of  sphygmograph  is  that  of  Dudgeon,  in  which 
the  straight  lever  is  supplanted  by  a  double-jointed  one  which  writes  on  a  horizontal  instead 
of  a  vertical  strip  of  smoked  paper.  The  tension  of  the  spring  pressing  down  the  pelotte 
is  roughly  adjustable,  which  allows  some  variation  in  the  pressure  over  the  artery. 
V.  J  a  q  u  e  t  has  improved  Dudgeon's  apparatus  by  adding  to  it  a  small  time  marker 
recording  fifths  of  a  second. 

Another  excellent  form  of  sphygmograph  is  that  devised  by  Roy  and  Adami,  which, 
by  means  of  a  dehcate  adjustment,  enables  the  observer  to  obtain  a  pulse  record  at 
exactly  diastolic  pressure.     Unfortunately,  it  has  never  been  placed  on  the  market,  and 

hence  has  not  been  subjected  to  the  test  of 
general  use,  but  any  one  who  is  interested 
in  sphygmographs  should  certainly  familiar- 
ize himself  with  their  observations. 


Fig.  33. — Brachial  pulse-curves  taken  with  the  Erlanger  blood -pressure  apparatus  from  the  arms 
of  two  patients,  merely  varying  the  pressure  in  the  cuff.  The  figures  indicate  the  pressures  at  which  the 
curves  are  taken,  those  underlined  indicating  maximal  and  minimal  pressures  respectively. 


Errors  in  Sphygmography. — In  spite  of  the  existence  of  these  fairly 
satisfactory  sphygmographs  and  of  their  wide  use,  discrepancies  between 
the  clinical  observations  and  the  tracings  obtained  are  so  great  that  Cabot 
refers  to  the  sphygmograph  as  "  an  interesting  little  toy."  The  reason  that 
it  is  not  of  value  must  be  either  that  the  apparatus  itself  is  subject  to 
inherent  errors,  or  that,  as  Mackenzie  states,  "  it  was  expected  to  give  in- 
formation of  a  kind  that  it  was  incapable  of  supplying."  Unfortunately, 
both  are  the  case. 

Athanasiu,  in  investigating  the  accuracy  of  graphic  recording  devices,  found  that  all 
sphygmographs  which  magnified  the  movement  more  than  twenty  times  introduced  a 
large  inherent  error,  that  of  all  the  forms  in  use  Marey's  introduced  the  least  error,  while 
the  Dudgeon  apparatus  and  the  Jaquet  magnified  it  1.30  times,  introducing  tremendous 
distortion  from  flinging  large  pulsations. 

On  the  other  hand,  the  writer,  D.  Gerhardt,  and  Stewart  have  been  able  to  show 
that  not  only  the  size  but  also  the  entire  type  of  the  pulse-curve  obtained  depends  upon 
the  pressure  exerted  upon  the  artery  and  other  similar  factors;  the  true  form  of  the  pulse- 
wave  being  obtained  only  when  the  pressure  exerted  by  the  sphygmograph  is  exactly  equal 


THE   ARTERIAL  PULSE. 


43 


to  the  pressure  within  the  artery.    Fortunately,  this  is  the  point  at  which  the  pulse  excur- 
sion is  maximal,  and  as  all  observers  strive  for  the  largest  excursion,  it  is  probable  that 
most  sphygmographic  records  are  taken  at  about  this  pressure.    The  ideal  apparatus  is 
the  one  in  which  it  is  not  merely  probable  but  certain,  and 
hence  that  of  Roy  and  Adami  is  the  only  one  which  abso- 
lutely fulfils  the  requirements. 

The  Absolute  Sphygmogram.  —  A  very  con- 
venient and  instructive  method  of  recording  pulse 
tracings  has  been  introduced  by  SahU.  Sahli 
transfers  the  pulse -curve  to  coordinate  paper 
upon  which  the  ordinates  represent  millimetres 
of  mercury  and  the  abscissae  represent  fractions 
of  a  second.  The  lowest  point  of  the  pulse-curve 
lie  marks  at  the  level  corresponding  to  the  mini- 
mal blood-pressure,  determined  at  the  time  with 
the  sphygmomanometer;  the  highest  point  at  the 
level  corresponding  to  the  maximal  pressure;  and 
maps  out  besides  this  the  other  main  points  of 
the  pulse-curve  (predicrotic  fall  and  wave,  dicrotic 
notch,  summit  of  dicrotic  wave,  etc.)  at  heights 
and  distances  proportional  to  their  occurrence  upon 
the  sphygmogram,  but  translated  to  this  new 
scale  of  pressure  and  time.  This  curve  he  terms 
the  absolute   sphygmogram. 

The  absolute  sphygmogram  can  also  be  read  off  from 
the  ordinary  sphygmogram  by  using  the  lowest  point  on 
the  tracing  as  the  ordinate  of  minimal  pressure  and  as  a 
the  pressure  at  other  points,  and  calculating  these  from  the 


Fig.  34.  — Absolute 
sphygmograms,  all  of  which 
correspond  to  the  radial  trac- 
ing above.  The  figures  to  the 
left  indicate  pressures  in 
ram.   Hg. 

base  line  for  determining 
proportion 


Ordinate   of    point   :    Total   height  of   pulse-wave  = 
Pressure  at  that  instant  (above  minimal  arterial  pressure)   :  Pulse-pressure. 

Discrepancies  between  Feeling  and  Recording  the  Pulse. — Not  all  the 

discrepancies  between  sensory  impression  and  sphygmogram  are  the  fault 
of  the  instrument.  In  the  first  place,  there  is  no  absolute  uniformity  in 
the  minds  of  physicians  as  the  standard  to  be  applied  to  the  individual 
pulse.  Thus,  the  writer  has  seen  one  eminent  clinician  dictate  a  note, 
^' pulse  not  collapsing,"  and  another  a  few  minutes  later  state  that  the 
same  "pulse  is  collapsing  in  quality."  The  pulse  had  not  changed,  but 
the  subjective  criteria  of  the  two  men  were  slightly  different. 

Again,  between  pulse  palpation  and  sphygmogram  there  is  a  difference.  It  is  very 
difficult,  almost  impossible,  to  determine  just  how  long  a  pulse  is  sustained  and  how  quickly 
it  falls,  since  these  judgments  are  based  upon  a  sequence  of  events  lasting  for  an  interval 
of  about  one-tenth  of  a  second,  and  changes  both  in  time  and  in  pressure  must  be  con- 
sidered without  the  presence  of  any  simultaneous  standard  for  comparison.  Psychologic- 
ally, such  comparisons  must  be  very  fallible.  Practically  they  are  not  as  fallible  as  they 
appear,  for  the  judgment  is  based  not  upon  form  or  duration,  unless  the  abnormalities  are 
marked,  as  much  as  upon  changes  of  pressure.  What  one  really  appreciates  most  in  feel- 
ing the  pulse  is  the  amount  of  minimal  pressure  ("hardness"  of  the  pulse)  and  the  amount 
of  the  pulse-pressure  (size  of  pulse),  and  only  to  a  lesser  extent  the  duration  of  the  pulse- 
wave.  Hence,  the  sensation  due  to  a  high  pulse-pressure  with  a  moderate  diastolic 
pressure  is  often  mistaken  for  that  due  to  a  collapsing  pulse,  though  the  form  of  the  pulse- 


44 


DISEASES   OF   THE   HEART    AND    AORTA. 


Fig.  35. — Significance  of  the  pulse-curve. 
/,  inflow  into  the  artery  from  heart;  O,  outflow 
from  the  artery  toward  the  periphery. 


wave  may  show  that  it  is  quite  well  sustained.  In  comparing  the  pulse  sensation  vnth  the 
sphygmograra,  one  is  therefore  comparing  two  somewhat  different  standards,  and  this 
inherent  difference  must  be  taken  into  account. 

Significance  of  the  Pulse=curve. — Assuming,  however,  that  one  has  ob- 
tained a  correct  tracing  from  the  artery,  what  deductions  are  allowable  ?  It 
is  evident  that  the  artery  expands  somewhat  under  an  increase  in  pressure 

(causing  a  rise  in  the  pulse-wave)  and 
contracts    when  pressure    decreases 
(causing    a    fall    in    the    pulse-wave). 
Further,  the  pressure  in  the  artery  in- 
creases or  decreases,  depending  upon 
whether  more  blood  enters  it  than  can 
leave  it  at  that  instant  (Fig.  35,  I  >  0) 
or   whether    the    reverse    is   the    case 
(I<0).     When    the   inflow   exactly 
equals  the  outflow  (1  =  0),  no  change 
of  pressure   occurs    and   a  plateau 
results.      The  pulse  tracing  is   merely  the   record   of  these  events  —  the 
record  of  the  ratio  that  the  inflow  into  the  artery  from  the  heart  bears 
to  the  outflow  toward  the  periphery  at  each  instant  of  the  cardiac  cycle. 

The  normal  pulse-wave  has  the 
following  forms:  an  upstroke  more 
or  less  steep  (percussion  wavej,  a 
rather  acute  summit,  and  sudden  fall 
(predicrotic)  followed  by  a  very  small 
rebounding  wave  (predicrotic  wave), 
then  another  more  gradual  fall  termi- 
nating in  a  small  notch  (dicrotic  notch) 
which  marks  the  end  of  systole 
(Marey,  Huerthle) ,  then  a  gradual  fall 
during  diastole.  In  the  aorta  the  fall 
in  waves  is  not  as  steep  as  in  the 
radial  artery,  which  indicates  that 
the  former  reflects  the  conditions 
near  the  heart,  the  latter  shows  the 
conditions  at  the  periphery  (Marey) 
Relation  of  Pulse  Form  to  Peri= 
pheral  Resistance. — There  are  three 
general  types  of  pulse  (Marey,  Hirsch- 
felder)  which  may  occur  without  any 
heart  lesion  whatever,  and  even  in  the  same  individual  at  the  same  maxi- 
mal and  minimal  pressures,  though  usually  the  maximal  and  minimal  pres- 
sures vary  with  these  conditions.     (Fig.  37.) 

Type  I  corresponds  to  marked  peripheral  dilata- 
tion, as  after  exercise,  after  meals,  in  shock,  fevers,  or  in  some  m  rvous 
individuals  with  vasomotor  instability.  This  is  the  collapsing  type  of  pulse, 
rapid  rise  and  rapid  fall  sometimes  followed  by  a  large  dicrotic  wave  (see 
page  45).  The  rise  is,  however,  about  two  hundredths  of  a  second  slower 
than  normal,  but  this  difference  is  not  within  the  limits  of  perception.     It 


■■■■■■■■■ 

illSSB!!! 

isaami 

iiaSSS!!! 

INTRAVENTRIC  '■  ( 
PRESSURE      / 

]!.===.= 

VENTRICULAR    i      / 
VOLUME            j^ 

H 

1 

Fig.  36. — Diagram  showing  the  time  rela- 
tions of  ventricular  volume  and  pressure  cur\-es 
to  pulse  tracings  from  tlie  aorta,  carotid  and 
radial  arteries.  Time  divisions  in  one-tenth  sec- 
onds. (Schematic.)  Dotted  lines  represent  curves 
taken  with  high  peripheral  resistance. 


THE    ARTERIAL   PULSE. 


45 


feels  more  sudden  because  it  is  sharply  followed  by  the  sudden  fall.  The 
fall  in  this  type  of  pulse  is  almost  complete  before  the  end  of  systole,  i.e., 
before  the  dicrotic  notch  which  marks  that  point  (Marey,  Huerthle). 


MO 


7S~^ — ^ 

Fig.  37. — Three  types  of  arterial  pulse-curve  corresponding  to  the  same  pulse-pressure  and  same  pulse- 
rate.    (Johns  Hopkins  Hosp.  Bull,  xviii.)    I,  vasodilation;    II,  normal;   III,  vasoconstriction. 

In  T  y  p  e  II  only  about  half  the  fall  occurs  during  systole.  This 
corresponds  to  moderate  degree  of  dilatation  and  is 
the  type  present  in  normal  individuals. 

In  T  y  p  e  III  the  wave  soon  rises  to  the  summit  and  remains  there, 
forming  a  sustained  plateau  (outflow  =  inflow)  until  the  end  of  systole,  when 
it  gradually  falls.  This  corresponds 
to  peripheral  constriction, 
preventing  the  outflow  from  the  aorta 
from  exceeding  the  inflow  into  it, 
as  is  the  case  where  a  normal  degree 
of  dilatation  is  present.  The  normal 
pulse  in  man  may  be  converted  into 
this  type  by  compression  of  both 
femoral  arteries  (Marey)  or  of  the  ab- 
dominal aorta  (Stewart).  The  mere 
increase  of  the  blood-pressure  is  not 
a  cause,  because  after  exercise  the 
blood-pressure  is  increased  and  yet 
the  pulse  becomes  more  collapsing 
than  before. 


;K./v^fv 


./VJv--N^ 


Fig.  38. — Effect  of  inhalation  of  amyl  nitrite 
upon  the  pulse-form.  (After  v.  Kries.)  Curves 
taken  in  succession.  Vasodilation  reaches  its 
maximum  at  c  and  diminishes  at  d  and  e.  Well- 
marked  dicrotism  at  d.  |3  and  a  indicate  second- 
ary waves  due  to  elasticity  of  the  artery. 


These  general  outlines  of  the  pulse- 
waves  are  further  modified  by  smaller  wave- 
lets due  to  the  elastic  vibrations  of  the  artery 
wall,  or  to  the  rebound  of  the  percussion 

wave  at  the  periphery  (v.  Kries).  The  most  important  of  these  is  the  dicrotic  wave 
following  immediately  upon  the  closure  of  the  aortic  valves  and  due  either  to 
a  centrifugal  wave  from  the  blood  impinging  against  them,  or  to 
a  reflected  centripetal  wave  from  the  periphery  toward  the 
heart  (v.  Kries).  Whichever  theory  may  be  correct,  the  essential  fact  remains  that 
the  dicrotic  wave  is  a  secondary  one  and  is  dependent  upon  arterial  elasticity.  V.  Kries 
has  shown  that  the  dicrotic  wave  is  most  marked  when  the  peripheral  vessels  are  consider- 
ably dilated,  but  not  when  they  are  dilated  to  their  fullest  extent  (Fig.  38). 

The  other  waves  may  occur  upon  either  upstroke  (anacrotic)  or  upon  the  downstroke 
(katacrotic,  Fig.  38,  a  .3)  and  are  designated  accordingly.     Small  secondary  waves  of  this 


46 


DISEASES   OF  THE   HEART   AND   AORTA. 


type  are  most  marked  when  the  pressure  is  high  and  the  heart  action  strong  {e.g.,  pulsus 
bisferiens),  but  their  occurrence  is  often  due  to  twitching  of  the  tendons  near  the  pelotte 
of  the  sphygmograph,  and  too  great  weight  must  not  be  attached  to  them. 


+ 


J)+  J)+  Hi^ 

Fig.  39. — Mercury  manometer  tracing  from  the  carotid  artery  of  a  dog,  showing  rhythmic  varia- 
tions in  blood-pressure  and  rhythmic  increase  in  dicrotism.  (Kindness  of  Prof.  Abel  and  Dr.  RowntreeJ 
The  dicrotic  wave  increases  at  the  points  (£)  +  )  at  which  the  blood-pressure  is  lowest  ( — )  and  the  peripheral 
arteries  are  dilated.     Time  in  seconds. 

Too  much  information  should  not  be  sought  from  the  sphygmogram. 
All  that  should  be  looked  for  is  whether  the  upstroke  is  sudden  (p.  celer) 
or  gradual  (p.  tardus) ;  whether  the  main  fall  in  the  wave  begins  early  or 
late  in  systole,  or  not  until  the  beginning  of  diastole;  also  whether  the 
fall  is  quite  or  nearly  complete  before  the  end  of  systole.      All  possible 

mental  reservations  should  be  made 
for  fling  of  the  lever,  incorrect  appli- 
cations of  sphygmograph,  etc.,  before 
a  judgment  is  made. 


NORMAL 

b.^--^--l>^-^-> 

NORMAL 

kMs-JViv^^^,, 

ANACROTIC — 

::xiMNiMK^- 

ANACROTIC 1 

1 
BI5FERIEN5^ 

TARDU5 -; 

TARDU5 . 

COLLAPSING— 

DICROTIC 

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_^;;^____^_^^^_,^^_^^ 

iJVkKJklvJ 

i .    '^-   [^    A   K  f\  f 

i^SHil^QIflSH^^^I 

■ 

THE   PULSE-RATE. 


The  normal  pulse  varies  consid- 
erably in  different  individuals,  being 
in  general  more  rapid  in  those  of 
small  stature  and  slower  in  persons 
of  larger  stature,  hence,  more  rapid 
in  women  than  in  men.  It  also 
varies  considerably  according  to  age, 
being  dependent  upon  the  relative 
tone  of  vagi  and  accelerators.  The 
pulse-rate  is  also  more  rapid  (tachy- 
cardia) in  fevers,  varying  in  general 
according  to  the  temperature — each 
degree  Fahrenheit  increase  corresponds 
to  an  acceleration  of  about  four  to  five 
beats  per  minute.  C.  D.  Snyder,  as 
the  result  of  a  long  series  of  experi- 
ments upon  the  heart-rate  in  different 
vertebrates,    finds    that    the    rate    is 

influenced  by  temperature  in  the  same  degree  as  is  the  velocity  of  simple 

chemical  reactions  and  follows  the  logarithmic  formula 


Fig.  40. — Diagram  showing  various  forms 
of  pulse-curve  encountered  clinically.  Systolic 
portions  of  the  curve  are  underlined.  HYPER- 
DICROT,  hyperdicrotic. 


_K,/   10    \ 

KoUi-to/ 


2    =  — 

In  typhoid  fever  there  is  often  an  exception,  a  temperature  of  103°  to  105°  being 
accompanied  by  a  pulse-rate  of  about  90  per  minute,  owing  to  a  toxic  stimulation  of  the 


THE    ARTERIAL   PULSE. 


47 


TYPES    OF    PULSE    IN    VARIOUS    DISEASES. 

The  following  types  of  pulse  are  associated  with  various  pathological 
conditions  and  corresponding  states  of  the  heart  and  vessels. 


Ml 

Clinical  condi- 

Blood-pressure associated  with  it. 

of  pulse.  1 

C 

Characteristics. 

tions  in  which  it 
is  most  fre- 

Vascular 
condition. 

0 

quently  observed. 

Maximum. 

Minimum. 

Pulse- 

J3 
CO 

pressure. 

Normal 

40 

Sudden  rise,  sharp 
apex,  slight  pre- 
dicroticfall;  then 

Normal    individ- 
uals 

Normal  . . 

Normal. 

slow    fall,    small 

Some  cases  of  aor- 

High  

Normal . . . 

Increased . 

Dilated. 

dicrotic    wave, 

tic  insufficiency 

gradual  fall  in  di- 

astole 

A  few  cases   of 
fever 

Normal  or 
d  i  m  in  - 
ished 

Pulse -rate 
qui  c  k- 
ened 

Dilated. 

Anacrotic . 

40 

Sudden     rise      or 

Arteriosclerosis; 

High 

High 

Slightly  in- 

Vasocon- 

slightly rounded 

chronic  nephritis 

creased 

striction. 

plateau  top  last- 

or    u  n  - 

mg  almost  to  di- 

Some  cases  of  aor- 

changed 

crotic    notch 

tic  insufficiency 

which    is    small; 

gradual  diastolic 
fall 

Some  normal  indi- 

Normal.  . . 

High 

Slightly  di- 

Vasocon- 

viduals 

minished 

striction. 

Bisferiens  . 

40 

Resembling     ana- 
crotic        except 
that    the    small 
predicrotic  fall  is 
followed  by  rise 

Arteriosclerosis; 
chronic  nephritis 

Hypertrophied 

High 

High 

Increased 

Vasocon- 
striction. 

heart  acting 

> 

equal    or    above 

strongly 

that  of  the  per- 

cussion  wave. 

making  the  sum- 
mit bifurcate 

Tardus 

40 

Gradual  slow  rise, 

Aortic  stenosis  . . . 

Slightly  or 

Elevated.. 

Increased 

Vasocon- 

percussion  wave 

greatly 

or   nor- 

striction. 

oblique,   summit 

elevated 

mal 

round,      gradual 
fall 

Collapsing. 

40 

Steep    rise,    apex 

Aortic  insufficien- 

Low    or 

Increased 

Vasodila- 

sharp,  sudden 

cy    (water-ham- 

normal 

tion. 

steep  fall,  di- 

mer or  Corrigan 

crotic    notch    in 

pulse) 

lower  half  of 

curve  often  level 

Fevers 

Normal  or 

Normal  or 

Normal  or 

Vasodila- 

after the  predi- 

low 

low 

increased 

tion. 

crotic  wave 

Normal      individ- 

Normal or 

Normal  or 

Normal  or 

Vasodila- 

uals, neuras- 

low 

low 

increased 

tion. 

thenics 

Some  cases  of 

Increased 

Slightly  in- 

Increased. 

Vasodila- 

Basedow's     dis- 

creased 

tion. 

ease 

Dicrotic.  .  . 

40 

Collapsing  in  qual- 

Fevers,  especially 

Normal  or 

Normal  or 

Normal  or 

Vasodila- 

ity  but  dicrotic 

typhoid 

subnor- 

s u  b  n  o  r- 

increased 

tion. 

wave  very   pro- 

mal 

mal 

nounced  and  pal- 

pable, as  a  small 

Normal  individ- 

Increased 

Normal  or 

Increased 

Vasodila- 

wave     regularly 

uals     during     or 

increased 

tion. 

following     soon 

after    exercise 

after  the  percus- 

sion wave 

Neurasthenics, 
after    amyl     ni- 
trite    or     nitro- 
glycerin 

Normal  or 
increased 

Normal.  .. 

Increased 

Vasodila- 
tion. 

Hyper- 
di  erotic 

40 

Dicrotic  wave  oc- 

Any of  the  condi- 

Normal or 

Normal . .  . 

Increased 

Vasodila- 

curs at  the  foot 

tions     in     which 

increased 

tion. 

of    the     ascend- 

dicrotism    may 

ing     instead     of 

occur,   but    with 

descending   limb 

more  rapid  pulse- 
rate. 

iFor  forms  of  ii  regular  pulse  see  page  63. 


48  DISEASES   OF   THE   HEART    AND    AORTA. 

vagus;  while  in  meningitis  the  high  intracranial  pressure  may  bring  the  rate  down  to  a 
great  deal  lower  (50  to  60)  and  may  cause  irregularity.  In  tuberculosis  the  pulse  is  rapid 
even  in  the  early  stages.  The  pulse-rate  is  also  accelerated  in  the  anaemias,  in  neuras- 
thenia, Graves's  disease,  hysteria,  shock  and  collapse,  abdominal  distention,  peritonitis 
and  other  diseases  of  the  abdominal  viscera,  and  in  numerous  cardiac  diseases.  In  fevers 
and  in  many  other  conditions  of  acceleration  the  pulse  becomes  extremely  small  and 
barely  palpable  on  the  one  hand,  and  extremely  rapid,  barely  countable  on  the  other — a 
small  and  "running"  pulse.  Pulse-rates  of  over  160  per  minute  are  not  uncommon  in 
fevers,  while  200  or  even  300  is  reached  in  paroxysmal  tachycardia.  At  these  great  rates 
the  duration  of  systole  is  markedly  shortened,  as  well  as  that  of  diastole  (the  period  of 
systolic  output  falUng  from  0.26  sec.  to  0.2  or  even  less). 

Slow  pulse  (bradycardia)  (below  60  per  minute)  is  observed  especially  in  conditions 
with  intracranial  tension,  in  meningitis,  in  digitalis  poisoning,  chronic  nephritis,  chronic 
myocarditis,  in  convalescence  from  some  fevers,  especially  diphtheria  and  influenza,  and 
in  Adams-Stokes  disease.  In  the  latter  condition  the  auricles  and  ventricles  are  beating 
independently  (see  chapter  on  Adams-Stokes  disease). 

BIBLIOGRAPHY. 

Pulse. 

Harvey,  W.:  Exercitationes  anatomicae  de  motu  cordis  et  sanguinis  circulatione,  Rotero- 

dami,  1671. 
For  historical   r^sum^  cf.   Morrow,  W.  S.:    "The  Pulse,"  Reference  Hand-book  of  the 

Medical  Sciences,  Phila.,  1903,  vi,  797. 
Vierordt,  K.:  Die  Lehre  vom  Arterienpuls,  Braunschweig,  1855. 
Marey,  E.  J. :  Recherches  sur  I'^tat  de  la  circulation  d'aprfes  les  caract^res  du  pouls  fournis 

par  un  nouveau  sphygmographe,  Journal  de  la  physiol.  de  I'homme,  Par.,  1860,    iii, 

241. 
V.  Jaquet,  A.:  Studien  ueber  graphische  Zeitregistrirung,  Ztschr.  f.  Biol.,  Muenchen  u. 

Leipz.,  1891,  xxviii,  N.  F.  x.,  1. 
Roy,  C.  S.,  and  Adami,  J.  G.:  Heart-beat  and  Pulse-wave,  Practitioner,  Lond.,   1890, 

xliv,  81,  161,  241,  347,  412,  xlv,  20. 
Athanasiu,  J.:  Methode  graphique,  Trav.  Assoc,  de  ITnstitut  Marey,  Paris,  1905,  p.  29. 
Hirschfelder,  A.  D.:  Graphic  Methods  in  the  Study  of  Cardiac  Diseases,  Am.  Jour.  M. 

Sci.,  Phila.,  1906,  cxxxii,  378. 
Gerhardt,  D.:  Beitrage  zur  Lehre  vom  Blutdruck,  Rindfleisch  Festschrift,  Leipz.,  1907. 
Stewart,  H.  A.:  An  Experimental  and  Clinical  Study  of  the  Blood-pressure  and  Pulse  in 

Aortic  Insufficiency,  Thesis,  Edinb.,  1907;  also  Arch.  Int.  Med.,  Chicago,  1908,  i,  102. 
Sahli,  H.:  Ueber  das  absolute  Sphygmogram  und  seine  klinische  Bedeutung  nebst  kriti- 

schen    Bemerkungen    ueber   einige    neuere    sphygmographische    Arbeiten,    Deutsch. 

Arch.  f.  klin.  Med.,  Leipz.,  1904,  Ixxxi,  493. 
Marey,  E.  J.:  La  circulation  du  sang  a  I'etat  physiologique  et  dans  les  maladies,  Par.,  1881. 
Huerthle,  K.:  Beitrage  zur  Haemodynamik,  Arch.  f.  d.  ges.  Physiol.,  Bonn,  1891,  xlix,  29. 
Hirschfelder,  A.  D.:Some  Observations  upon  Blood-pressure  and  Pulse  Form,  Bull.  Johns 

Hopkins  Hosp.,  Baltimore,  1907,  xviii,  262. 
V.  Kries,  J.:  Studien  zur  Pulslehre,  Freiburg,  1892. 
Snyder,  C.  D.:  The  Influence  of  Temperature  upon  the  Rate  of  the  Heart-beat  in  the 

Light   of   the  Law  for  Chemical    Reaction  Velocity,  Am.  J.  Physiol.,  Bost.,  1906, 

xvii,  350. 


IV. 

THE   VENOUS    PULSE    AND    ELECTROCARDIOGRAM 
IN    HEALTH   AND    DISEASE. 

THE  NORMAL  VENOUS  PULSE. 

As  has  been  seen,  the  study  of  the  blood-pressure  and  of  the  arterial 
pulse  conveys  information  regarding  the  strength  of  the  heart-beat,  the 
condition  of  the  peripheral  arteries,  and  the  velocity  which  the  heart  is 
imparting  to  the  blood  stream.  But  it  reveals  the  action  of  the  left  ven- 
tricle only,  and  what  occurs  in  the  other  chambers  of  the  heart  must  be 
sought  for  elsewhere. 

In  studying  the  heart  from  the  four  stand-points  of  Engelmann, 
rhythmicity,  irritability,  conductivity,  and  contractility, 
it  is  necessary  to  obtain  a  knowledge  of  the  origination  of  the  impulses 
in  or  above  the  right  auricle  (atrium),  of  whether  impulses  other  than 
those  causing  the  normal  rhythm  are  acting  upon  that  chamber,  of  whether 
the  right  auricle  (atrium)  is  itself  contracting,  and  of  whether  all  the 
impulses  are  being  properly  conducted  to  the  ventricle.  Our  knowledge 
upon  these  points  has  been  derived  almost  entirely  from  the  study  of  the 
pulsation  in  the  jugular  vein. 

Visible  Pulsation  in  the  Veins. — Pulsation  over  the  veins  is  visible  in 
80  per  cent,  of  healthy  individuals  (Hewlett)  and  is  as  pronounced  as  that 
over  the  arteries,  but  it  is  different  in  character.  The  latter  shows  the  force- 
pump,  the  former  the  suction-pump  action  of  the  heart.  The  pulsation  over 
the  arteries  is  quick,  sharply  localized,  easily  palpable,  and  the  impulse  is 
more  marked  than  the  collapse;  that  over  the  veins  is  diffuse,  wavy,  rarely 
palpable,  and  the  collapse  is  more  marked  than  the  im- 
pulse itself.  Further,  the  pulsations  over  the  vein  under  normal  con- 
ditions are  exactly  twice  the  number  of  those  seen  over  the  artery,  and  the 
first  of  the  collapses  is  synchronous  with  the  impact  in  the  artery.  Such  a 
pulsation  over  the  vein  is  known  as  the  "physiological,"  "negative,"  or 
''double"  venous  pulse,  in  contradistinction  to  the  other  types  of  venous 
pulse  to  be  described  later. 

The  pulsation  over  the  veins  is  not,  like  the  arterial  pulse,  to  be  seen 
in  every  vein  in  the  body,  though  Morrow  has  shown  that  in  dogs  it 
can  be  detected  by  means  of  delicate  manometers.  To  the  eye  and  to 
the  recording  apparatus  available  upon  man,  it  is  appreciable  only  in  the 
veins  near  the  heart,  the  external  and  internal  jugular,  the  cephalic,  and 
the  axillary.  Occasionally  it  is  also  to  be  seen  in  the  brachiocephalic  and 
other  veins  in  the  arm.^  The  site  where  it  is  most  easily  and  uniformly 
seen  is  in  the  right  supraclavicular  fossa,  either  over  or  just  to  the  right  of 

'  Friedreich  thought  that  this  pulsation  was  transmitted  from  the  arteries  through 
the  capillaries  to  the  veins,  but  such  transmission  probably  never  takes  place  and  other 
explanations  must  be  sought. 

4  49 


50  DISEASES   OF   THE    HEART    AND    AORTA. 

the  origin  of  the  sternocleidomastoid.  Sometimes  it  is  a  httle  more  marked 
in  the  supraclavicular  fossa  at  about  the  mammillary  line  where  the  exter- 
nal jugular  vein  enters  the  subclavian.  The  normal  venous  pulsation  is 
rarely  to  be  seen  when  the  subject  is  standing  or  when  propped  up  high 
upon  pillows,  but  is  most  distinct  after  he  has  been  in  reclining  posture 
for  some  minutes  with  a  single  pillow  under  his  head  and  neck.  In  patients 
with  venous  stasis,  on  the  other  hand,  it  may  be  necessary  for  the  patient 
to  sit  upright  before  any  undulations  appear. 

It  must  be  borne  in  mind  that  the  pulsation  seen  and  recorded  over 
the  veins  represents  the  alternate  filling  and  collapse  of  the  latter.  The 
collapse,  that  is  the  obliteration  of  the  lumen  of  the  vein  by  the  atmospheric 
pressure,  is  usually  the  most  important  factor.  It  is  evident  that  a  wave 
will  occur  during  those  periods  in  which  the  pressure 
within  the  vein  is  greater  than  the  atmospheric,  and  a 
collapse  will  occur  whenever  it  is  less.  If  it  is  permanently  less 
(negative) ,  the  vein  will  remain  collapsed ;  if  it  is  permanently  a  little  greater, 
the  vein  will  remain  distended.     In  neither  case  will  a  pulsation  be  seen. 

The  normal  pulsation  is  best  seen  when  the  pressure  in  the  jugular  vein  is  alternating 
between  a  positive  and  a  negative  pressure  during  the  different  phases  of  the  cardiac 
cycle.  The  elastic  distention  of  the  vein  is  not  called  into  play.  The  elastic  distention  of 
the  vein  at  systole  occurs  only  at  a  much  higher  venous  pressure,  as  in  tricuspid  insuffi- 
ciency. Occasionally,  especially  in  chronic  heart  cases  with  phlebosclerosis,  the  veins  stand 
out  like  large  knotty  cords,  but  no  pulsation  is  to  be  discerned  in  them  at  all.  The  knotty 
appearance  (Fig.  41)  is  due  to  the  closure  of  the  valves  within  the  veins,  the  dilatations 
appearing  just  above  the  valves.  Perhaps  the  closure  of  the  valves  prevents  or  dampens  the 
pulsation,  or  perhaps  the  rigidity  of  the  vessel  wall  prevents  it  from  collapsing  and  filling. 
Normally  the  valves  in  the  jugular  do  not  close,  but  this  closure  is  brought  about  by  chronic 
venous  stasis,  just  as  it  is  in  quadrupeds  where  back  pressure  results  from  the  head  being 
dependent.  In  such  cases  it  is  impossible  to  obtain  any  idea  of  the  undulations  nearer  the 
heart. 

GRAPHIC  RECORDS  OF  VENOUS  PULSATIONS. 

A  far  more  exact  idea  of  the  nature  of  the  jugular  pulsation  can  be 
obtained  by  recording  it  graphically  than  by  mere  inspection.  With  proper 
apparatus  this  is  not  accompanied  by  any  difficulty,  and  a  satisfactory 
record  of  both  venous  and  carotid  pulsations  can  be  obtained  in  about  the 
same  time  as  a  radial  sphygmogram.  For  the  interpretation  of  the  venous 
tracing  it  is  necessary  to  compare  it  with  the  other  events  of  the  cardiac 
cycle,  which  is  accomplished  by  using  the  pulse-wave  from  some  artery 
to  fix  the  standard  of  time. 

In  order  to  interpret  the  waves  upon  the  venous  pulse,  it  is  necessary 
to  record  simultaneously  the  venous  pulse  and  either  the  arterial  pulse  or 
the  cardiogram,  and  to  see  at  which  point  in  the  cardiac  cycle  each  event 
will  fall.  Accordingly,  all  forms  of  apparatus  (polygraph)  for  obtaining 
such  records  are  arranged  for  taking  at  least  two  records  simultaneously. 
In  all  of  these  the  pulsation  from  over  the  vein  is  received  in  the  same  way, 
and  the  only  difference  in  the  various  forms  of  polygraph  lies  in  the  method 
of  obtaining  the  arterial  tracing  and  in  the  form  of  kj^mograph  used. 

Application  of  the  Receivers. — ^The  pulsation  in  the  jugular  vein  is  recorded  by 
holding  over  the  skin  above  it  a  small  glass  funnel  on  special  receiver  (Fig.  41,  c),  which  i& 
connected  with  a  Marey  recording  kymograph  tambour.    The  movements  of  the  skin  are 


THE  VENOUS  PULSE  AND   ELECTROCARDIOGRAM.        51 

transmitted  at  once  to  the  kymograph  tambour  and  recorded  by  the  lever.  As  a  rule,  the 
most  favorable  conditions  are  obtained  when  the  patient  is  lying  with  head  and  neck 
supported  on  a  single  pillow  that  extends  down  just  to  the  shoulders,  with  his  head  turned 
well  to  the  right  and  the  neck  definitely  flexed.  In  this  way  the  right  sternocleidomastoid 
is  relaxed  and  a  tracing  over  the  pulsation  from  base  of  the  internal  jugular  vein  is  trans- 
mitted to  the  skin.  When  this  is  not  obtainable  the  junction  of  the  external  jugular  vein 
with  the  subclavian  should  be  tried  in  the  same  way.  The  funnel  should  be  pressed  against 
the  skin  just  enough  to  make  the  contact  air- 
tight without  affecting  the  pulsation,  but  this 
is  effected  without  any  great  dexterity,  and 
oscillations  due  to  the  holding  of  the  re- 
ceiver rarely  appear  upon  the  tracing.  When 
they  do  so  it  is  in  the  form  of  fine  oscillations 
bearing  no  relation  to  the  cardiac  cycle  and 
having  a  rate  of  from  four  to  eight  per 
second,  in  contrast  to  the  much  slower  and 
larger  movements  in  the  veins.  Such 
tracings  should  be  discarded. 

In  many  cases  the  simple  glass  funnel 
is  not  as  satisfactory  as  a  receiving  device 
introduced  by  Mackenzie  (Fig.  41,  c),  con- 
sisting of  a  shallow  metal  pan  3  cm.  in 
diameter  with  a  tube  leading  off  from  it  in 
the  form  shown  in  Fig.  41,  one  portion  of 
the  circumference  being  flattened  instead 
of  round  in  order  to  fit  closely  above  the 
clavicle.  It  is  convenient  to  have  a  small 
hole  in  the  top  of  the  pan  so  that  it  may 
be  adjusted  to  the  skin  without  moving 
the  recording  lever,  and  after  adjustment 
is  complete  the  hole  is  closed  by  placing 
the  finger  over  it. 

The  tracing  from  the  carotid  artery  is 
obtained  in  a  similar  way,  using  for  a 
receiver  a  small  tambour  surmounted  by  a 
button  to  fit  over  the  artery  (Fig.  41,  d). 
A  small  hole  in  the  top  of  this  tambour 
serves  the  same  purpose  as  before  and  is 

also  stopped  by  covering  -with  the  finger.  The  carotid  artery  is  next  to  the  skin  just 
inside  the  sternocleidomastoid  when  the  head  is  turned  toward  the  corresponding 
side,  the  pulsation  being  most  marked  when  the  receiver  is  pressed  heavily  upon  it. 

Comparison  of  Carotid  and  Jugular  Pulsation. — Since  the  jugular  vein 
and  the  carotid  artery  are  at  about  the  same  distance  from  the  heart,  the 
tracings  from  the  latter  must  always  be  compared 
with  the  former  in  order  to  exclude  waves  which  might  have  been 
transmitted  to  it  from  the  artery,  and  also  to  indicate  the  relations  of  the 
venous  waves  to  the  cardiac  cycle.' 

This  comparison  may  be  made  by  taking  the  jugular  and  the  carotid  tracings  simul- 
taneously and  comparing  them  with  each  other  directly,'  or,  for  the  sake  of  convenience, 


nUIVUIfOli  «LIN 


KaivitFORMnun 


Fig.  41. — Sites  for  recording  the  jugular  and 
carotid  pulsations.  A,  distribution  of  the  veins 
(shaded  in  black),  showing  the  sites  for  applying  the 
jugular  receiver  (truncated)  and  the  carotid  receiver 
(concentric  circles);  B,  appearance  of  the  valves 
within  the  jugular  vein  when  closed  by  back  pres- 
sure; C,  receiver  for  jugular  vein;  Z),  spring  tambour 
for  recording  the  pulsation  over  the  carotid  artery. 


*  Where  great  accuracy  is  necessary  the  onset  of  the  c  wave  must  be  compared  with 
that  of  the  apex  beat. 

'  It  is  not  necessary  that  the  levers  be  exactly  superposed,  but  it  is  preferable  to 
measure  off  the  distance  of  the  given  point  horizontally  from  the  arc  described  by  the 
lever  at  the  beginning  of  the  tracing  (e.g.,  Fig.  44).  This  distance  is  then  laid  off  upon  the 
other  curve  in  the  same  manner.  Wherever  the  curve  may  begin  the  paper  traverses  the 
same  distance  upon  both  curves  in  the  same  time. 


52 


DISEASES   OF   THE    HEART   AND    AORTA. 


Fig.  42. — Apparatus  for  recording  the  re.spiration. 
RUB,  rubber  tube;  GL,  glass  tube. 


a  carotid  and  a  brachial  or  radial  tracing  may  be  made  simultaneously,  and  the  point  at 
which  the  carotid  wave  begins  marked  off  upon  the  latter.  Then  a  jugular  and  a  brachial 
tracing  may  be  made,  and  the  time  that  the  carotid  wave  occurs  before  the  brachial  marked 
off  before  each  brachial  wave  in  this  tracing,  and  these  points  then  measured  off  upon  the 
jugular  tracing.    This  is  often  the  simplest  and  quickest  procedure. 

Respiration  Recorder. — It  is  often  of  importance  to  determine  the 
relation  of  an  arrhythmia  to  the  phases  of  respiration.  The  simplest  device 
for    recording   the    latter  consists   of  a    piece    of   rubber    tube    (Fig.   42, 

rub)  connected  with  the  tube  to 
the  recording  tambours  by  a  short 
L-shaped  piece  of  glass  tubing 
(gl).  A  piece  of  string  or  tape  is 
attached  to  the  rubber  tube, 
another  to  the  glass  tube.  The 
apparatus  is  then  put  on  so  as 
to  encircle  the  level  of  the  nip- 
ples. The  strings  are  tied  tightly 
enough  to  just  stretch  the  rubber 
tube  during  expiration.  Inspira- 
tion then  causes  a  downstroke  of 
the  levers,  expiration  an  upstroke. 

Forms  of  Polygraph. — Several  forms  of  polygraph  for  clinical  purposes  have  been 
devised  to  record  these  curves.  Their  relative  value  depends  largely  upon  the  delicacy  of 
the  tambours.  The  oldest  form  is  the  polygraph  of  Marey,  consisting  of  an  ordinary  kymo- 
graph drum  arranged  to  rotate  horizontally 
with  two  Marey  tambours  to  write  upon  it, 
so  as  to  record  simultaneously  the  curve 
from  the  jugular  and  carotid  or  jugular  and 
cardiogram.  This  is  fairly  satisfactory,  but 
in  mechanical  perfection  some  others  are 
superior.  Mackenzie  has  devised  two  forms 
of  polygraph.  The  first,  a  simple  Jaquet 
sphygmograph  upon  which  a  Marey  tambour 
is  mounted  in  addition  so  as  to  record  the 
radial  pulse  and  jugular  or  carotid,  etc., 
simultaneously,  the  time  being  marked  off 
in  i  seconds  by  a  small  clock-work  as  well. 
In  the  improved  form  of  Mackenzie  poly- 
graph, the  levers  bear  ink  pens  and  write 
upon  an  endless  roll  of  white  paper,  so  that  a 
very  long  series  can  be  obtained.  V.  Jaquet's 
cardiosphygmograph  differs  from  the  simple 
sphygmograph   only  in   bearing  in  addition 

two  Marey  tambours  whose  double-jointed  levers  write  just  above  the  lever  attached  to 
the  radial  pelotte.  Both  Mackenzie's  and  Jaquet's  methods  suffer  from  the  inconvenience 
of  adjusting  the  sphygmograph  to  the  radial  artery  and  keeping  it  adjusted  during  the 
entire  observation,  a  factor  which  is  very  disconcerting  to  both  patient  and  physician  and 
which  prevents  many  important  observations  from  being  taken  on  restless  patients. 

This  difficulty  is  obviated  in  the  writer's  modificaton  of  the  Er- 
langer  blood-pressure  apparatus  (Fig.  22,  page  21),  in  which  two  small 
Marey  tambours  and  a  time-marker  are  arranged  to  write  above  the  lever  of  the  blood- 
pressure  apparatus.  When  the  bag  is  inflated  upon  the  arm,  the  brachial  pulse  is  recorded 
by  the  lever  of  the  blood-pressure  apparatus  and  used  as  the  standard  instead  of  the  radial 
pulse.  This  entails  no  trouble  and  no  expenditure  of  time,  thereby  saving  much  of  the 
trouble  given  by  the  other  methods,  and  permits  a  set  of  records  to  be  obtained  very 


Fio.  43. — ^V.  Jaquet's  cardiosphygmograph. 
(Kindness  of  A.  H.  Thomas  Co.)  a,  time  marker 
(s  sec);  b,  c,  levers  of  tambours  for  recording 
venous  tracing,  carotid  pulse,  or  cardiogram;  d, 
lever  recording  radial  pulse-wave. 


THE   VENOUS   PULSE  AND   ELECTROCARDIOGRAM. 


53 


quickly.  It  is  also  possible  for  the  operator  to  work  with  one  hand  free  and  thus  save  the 
necessity  of  an  assistant.  The  curve  thus  obtained  from  the  jugular  vein  is  shown  in 
Fig.  44  and  its  relation  to  the  other  events  in  the  cardiac  cycle  shown  in  Fig.  45. 


SLOW 

FAST 

CAROTID 

^V 

c  d  c  d   c  d 

.TV.^ 

'c          d                       c     ' 

JUGULAR 

IW 

ksU 

ill 

BHH^B 

c  d           c  d 

^                                Bard 

JUGULAR 


CAROTID 


AURICULAR  CONTRACT 


INTRAVENTRICUUR 
PRESSURE 


VENTRICULAR 
VOLUME 


SOUNDS 


A 


E 


ELECTRO 
CARDIOGRAM 


m^ 


Fig.  44. — Normal  venous  tracings,  a,  wave  due  to  auricular  contraction;  c,  wave  at  onset  of 
ventricular  contraction  (the  vertical  line  c  representing  the  beginning  of  the  carotid  pulse-wave);  x,  the 
bottom  of  the  mesosystolic  collapse;  d  time  of  dicrotic  notch  in  the  carotid;  v,  wave  at  end  of  systole; 
y,  hollow  at  the  end  of  the  postsystolic  collapse;  t,  d  (Bard),  telesystolic  and  protodiastolic  waves 
described  by  Bard.     (The  x  and  y  depressions  are  not  lettered  on  all  tracings.) 

Recently,  Uskoff  has  constructed 
a  very  compact  form  of  this  appara- 
tus, bearing  an  Erlanger  blood- 
pressure  apparatus,  a  tambour  for 
recording  the  height  of  the  blood- 
pressure  objectively,  a  tambour  for 
apex  or  venous  or  carotid  tracings, 
and  an  excellent  time-marker.  This 
seems  to  be  a  very  good  instrument  of 
wide  applicability,  suitable  to  all  the 
needs  of  the  practitioner. 

The  choice  of  apparatus 
depends  chiefly  upon  the  deli- 
cacy of  the  tambours  and  upon 
the  portableness  of  the  appara- 
tus. In  the  latter  regard  the 
Jaquet  cardiosphygmograph  is 
particularly  desirable,  but  in 
the  former  it  is  excelled  by 
many.  The  possession  of 
extremely  delicate  tambours 
enables  the  observer  to  proceed 
rapidly  and  to  obtain  beautiful 
and  accurate  records  which 
would  be  impossible  with  ordi- 
nary apparatus.  The  horizon- 
tally writing  tambours  of 
French  manufacture  are  partic- 
ularly delicate. 


MITRAL  a  TRICU5' 
A(J8T/C&  PULMONIC 

Fig.  45. — Diagram  representing  the  various  events  in 
a  cardiac  cycle.  Letters  as  in  previous  figures.  Time  in 
tV  seconds  (vertical  lines).  Dotted  lines  represent  curves 
obtained  when  the  peripheral  resistance  is  high.  The 
pulse  becomes  anacrotic  and  the  intraventricular  increases 
toward  the  end  of  systole. 


INTERPRETATION    OF    WAVES    UPON    THE    VENOUS    TRACING. 

The  curve  of  venous  pressure  obtained  clinically  and  in  animals  (Fred- 
ericq,  Morrow,  Hering,  Theopold)  corresponds  exactly  to  those  obtained 
within  the  auricles  (Chauveau  and  Marey,  Fredericq,  Porter).    The   first 


64 


DISEASES   OF   THE   HEART    AND    AORTA. 


wave  (a) 'in  the  venous  pulse  is  due  to  the  contraction  of  the  right 
auricle,  and  disappears  when  the  auricle  is  paralyzed.  It  occurs  about 
one-fifth  second  before  the  contraction  of  the  ventricle.  The  onset  of  the 
ventricular  contraction  is  marked  on  the  venous  tracing  by  a 
small  wave  (c),  caused  in  part  by  the  pushing  up  of  the  tricuspid  valve 

when  the   intraventricular  pressure  rises 

(Hirschfelder,  1.   c,   Bard,  1.  c.  Morrow, 

JUG.  ^Bfil^B^RIKBBiil^^H^M^B      Cushny  and  Grosh),  and  in  part  by  the 

flow  of  blood  from  the  coronary   veins, 
which,  as  Porter  has  shown,  are  forcibly 
emptied   into  the  auricle   at  this  instant 
(Sewall  and   Hirschf elder) .     Mackenzie 
thinks  that  it  is  due  only  to  the  carotid 
pulsation    transmitted    to    the   vein,   but 
Morrow  has  obtained  it  after  ligature  of 
the  carotid  in  animals.     Besides  the  wave 
appears  about  ^V  second  before  the  ca- 
rotid wave  in  many  cases  (Hirschfelder, 
Bard).     When   the  tracings  are  taken   from  the   left  jugular   and  right 
carotid,  the  c  wave  in  the  vein  may  be  later  than  that  in  the  arter}%  owing  to 
longer  time  of  transmission.     The  c  wave  is  almost  always  present;  but,  as 
Bard  has  shown,  it  may  be  very  small  or  entirely  absent  in  hearts  whose  ven- 
tricles are  failing  (Fig.  46) .     The  rise  of  the  c  wave  is  followed  by  a  large 
if  a  1 1  (x),  which  may  be  the  largest  fall  of  pressure  in  the  whole  cardiac 
jcycle.     The  exact  mechanism  by  which  this  fall  of  pressure  in  the  veins 
;(and  also  in  the  auricles)  is  produced,  and  especially  why  it  should  sometimes 
represent  the  largest  fall  of  pressure,  is  not  clear.     It  is  evident  at  this  period 
of  the  cycle  that  several  events  are  taking  place:  (1)   relaxation  of  the 
auricle ;  (2)  a  certain  amount  of  downward  pull  which  the  papillary  muscles 


Fig.  46. — Venous  tracing  showing  ab- 
sence of  the  c  wave  in  a  case  of  heart  fail- 
ure. The  tracing  is  otherwise  normal. 
JUG.,  right  jugular  vein;  CAR.,  left  ca- 
rotid artery.    Time  in  I  seconds. 


Fig.  47.- 


-A.  Venous  tracing  showing  auricular  paralysis  (absence  of  a  wave)  with  large  (x)  depression 
during  ventricular  systole  between  c  and  v.     B.  Same  tracing,  faster  speed. 


exert  upon  the  tricuspid  and  mitral  valves;  (3)  at  each  systole,  as  can  be 
seen  when  the  heart  is  exposed,  the  movements  of  the  latter  within  the  chest 
are  exerting  a  pull  upon  the  venae  cavse,  thus  pumping  their  contents  into 
the  auricles;  (4)  the  outflow  of  blood  and  the  decrease  in  size  of  the  heart 
during  systole  cause  a  slight  increase  in  the  negative  pressure  within  the 


*  Since  Mackenzie's  first  nomenclature  and  lettering  of  the  waves  was  introduced,  a 
great  variety  of  lettering  and  of  designation  by  numerals  has  been  used  by  different  authors; 
but  these  serve  to  compHcate  rather  than  to  simplify  the  question.  The  letters  or  numbers 
are  merely  symbols,  and  a  single  uniform  system  would  be  better  than  a  Babel  of  terms. 


THE   VENOUS   PULSE    AND   ELECTROCARDIOGRAM.        55 

thorax  which  may  be  transmitted  to  the  thin-walled  veins.  It  is  probable 
that  neither  of  these  factors  alone  is  responsible  for  the  fall  (x  depression), 
but  that  each  is  active.  Certain  it  is  that  auricular  relaxation  is  not  the 
sole  cause,  for  as  shown  in  Fig.  47  it  may  still  be  the  largest  depression  in 
cases  in  which  the  auricle  is  paralyzed. 

Dr.  Peabody  has  called  the  writer's  attention  to  a  small  wave  which  is  frequently 
seen  during  midsystole,  especially  in  tracings  from  vigorous  hearts,  occurring  just  at  the 
base  of  the  x  depression,  and  which  in  many  cases  cannot  be  due  to  fling  of  the  lever.  The 
origin  and  significance  of  this  wave  are  extremely  uncertain.  It  may  be  reaUy  transmitted 
from  the  artery;  or,  as  Dr.  Peabody  suggests,  may  be  due  to  slight  insufficiency  of  the 
papillary  muscles  studied  by  Sewall. 

The  fall  which  leads  to  the  x  depression  usually  lasts  until  about  the 
end  of  ventricular  systole,  d  (instant  of  the  dicrotic  notch),  after  which  it 
is  followed  by  a  large  rise  (diastolic  wave  of  Porter;  v  or  ventricular  wave 
of  Mackenzie;  vs,  ventricular  stagnation  (Ventrikelstauungswelle) ,  Hering; 
telesystolic  wave,  t,  Bard).  This  wave  is  very  constant  in  its  occurrence 
and  is  usually  supposed  to  represent  stagnation  within  the  ventricle  lasting 
from  the  end  of  systole  until  the  tricuspid  valve  opens;  the  fall  v-y  indi- 
cates the   opening   of   the   tricuspid   valve. 

As  Bard  has  shown,  two  undulations  are  occasionally  found  (t,  d;  t,  telesystolic, 
occurring  at  the  end  of  systole;  and  d,  protodiastolic,  occurring  at  the  very  beginning  of 
diastole).  Bard  states  that  the  wave  t  is  coincident  with  the  first  secondary  (predicrotic) 
wave  of  the  arterial  pulse,  the  second  with  the  vibration  of  the  ventricles  due  to  the  clos- 
ure of  the  aortic  valves,  but  this  is  not  very  satisfactory. 

Sewall  believes  that  the  stagnation  at  the  end  of  systole  (when  the  upstroke  of  the 
V  or  t  wave  occurs  before  the  end  of  systole)  is  due  to  a  fatiguing  or  stretching  of  the  papil- 
lary muscles,  causing  a  slight  tricuspid  regurgitation  at  that  instant;  but  in  cases  with  no 
murmur  in  the  tricuspid  region  this  explanation  needs  confirmation. 

The  rise  upon  the  v  wave  outlasts  the  end  of  systole  by  about  yV  sec, 
which  probably  represents  the  time  required  to  transmit  this  change  of 
pressure  to  the  veins. 

Most  writers  follow  Mackenzie  in  believing  that  the  upstroke  of  the  v  wave  repre- 
sents stasis  within  the  ventricle  lasting  until  the  tricuspid  valve  opens,  but  cardiometer 
tracings  show  that  filling  of  the  ventricles,  or  at  least  dilatation,  begins  at  the  instant 
systole  ends.  Chauveau's  tracings  of  the  movements  of  the  heart  valves  also  show  that 
the  triscupid  valve  opens  before  the  time  at  which  the  crest  of  the  v  wave  appears,  so  that 
it  is  probable  that  this  wave  does  not  represent  the  very  instant  at  which  the  tricuspid 
valve  opens,  but  that  when  the  period  x-v  exceeds  the  transmission  time  the  interval 
represents  a  period  during  which  the  venous  pressure  remains  greater  than  atmospheric 
pressure.  Or  it  may  last  until  a  sufficient  amount  of  blood  has  entered  the  ventricle  to 
have  relieved  the  venous  engorgement  which  followed  the  cessation  of  the  factors  which 
had  produced  the  x  depression. 

The  descending  limb  of  the  v  wave  continues  as  long  as  blood  is  rushing 
in  to  fill  the  ventricle  (Henderson's  period  of  diastolic  filling),  after  which 
there  is  a  gradual  filling  of  the  vein  and  a  rise  until  the  next  auricular  systole. 
In  slow  hearts  Hirschf elder  and  A.  G.  Gibson  have  shown  that  the  inflow 
into  the  auricles  and  the  filling  of  the  veins  is  no  longer  uniform  but  is  inter- 
rupted by  a  well-defined  wavelet  {h,  Hirschf  elder;  h,  Gibson)  which  follows 
the  V  wave  by  a  definite  interval  (Fig.  48,  h) .    Both  these  writers  indepen- 


56 


DISEASES   OF   THE    HEART   AND    AORTA. 


dently  ascribed  this  wave  to  the  snapping  together  of  the  auric- 
ulo  ventricular  cusps  at  the  end  of  ventricular  fill- 
in  g  in  middiastole,  and  the  former  called  attention  to  its  correspondence 


'  ^  c   '^d 


Fig.  48. 


-Venous  tracing  from  a  very  slow  heart,   with  loud  third  heart  sound,  showing  the  presence 
of  the  h  wave.    Max,  maximal  blood-pressure;  Min,  minimal  blood-pressure. 


with  the  onset  of  Henderson's  period  of  diastasis.    This  fact  is  further  borne 
out  by  the  presence  of  a  corresponding  wave  upon  the  tracing  from  the 

oesophagus  (Fig.  54,  h).  This  wave 
disappears  when  the  pulse-rate  be- 
comes more  rapid   (Fig.  49). 


G.  A.  Gibson,  Eyster,  and  the  writer 
have  occasionally  seen  a  wave  w  in  late  diastole 
of  slow  pulse  preceding  the  wave  of  auricular 
contraction  (a  wave)  by  a  rather  definite 
interval  (Fig.  50).  The  distance  from  the  h 
wave  varies.  This  wave  is  assumed  by  the 
former  writer  to  represent  a  contraction  origi- 
nating in  the  sinus  region  of  the  heart.  Since 
the  remnant  of  the  embryonic  sinus  is  actually  incorporated  within  the  body  of  the  auricle 
(atrium),  this  view  is  questionable  and  requires  experimental  confirmation. 


Fig.  49. — ^Tracing  from  the  same  person 
one  hour  later,  after  giving  atropine  and  quick- 
ening the  pulse.    The  h  wave  is  absent. 


Fig.  50. — Showing  a  wave  w  occurring  shortly  before  the  a  wave.     (From  a  tracing  made  in  collaboration 

with  Prof.  L.  F.  Barker.) 


VISUAL    EXAMINATION    OF    THE    VENOUS    PULSE. 

Some  of  these  events  in  the  cardiac  cycle  may  be  clearly  distinguished 
with  the  naked  eye.  Upon  looking  carefully  at  the  jugular  pulsation  in  a 
normal  individual  and  placing  the  finger  upon  the  carotid  artery  the  vein  will 
be  seen  to  fill  twice  (a  wave  and  v  wave)  and  to  collapse  twice  (x  depression 
and  y  depression)  for  each  beat  felt  in  the  carotid  artery  ("  presystolic-dias- 
tolic," "physiological,"  "negative,"  "double"  venous  pulse  (Hirschf elder)). 
These  waves  may  be  timed  less  accurately  with  the  eye,  but,  although,  as 
Mackenzie  states,  visual  examination  may  save  the  examiner  many  unnec- 
essary tracings,  it  should  not  be  relied  upon  in  doubtful  cases.  For  example, 
a  simple  mesosystolic  collapse  (like  that  shown  in  Fig.  44)  with  absolute 
paralysis  of  the  auricles  may  simulate  a  normal  venous  pulse. 


THE  VENOUS  PULSE  AND  ELECTROCARDIOGRAM. 


57 


ABNORMAL  TYPES  OF  VENOUS  PULSE. 


Auricular  Paralysis. — Besides  this  normal  (negative  or  double  venous) 
pulse  several  other  types  of  venous  pulse  are  seen.  In  venous  stasis  and 
cardiac  failure  the  auricles  may  soon  become  weakened  and  the  a  wave,  due 
to  their  contraction,  may  disappear  entirely  (Figs.  47  and  51).    This  phe- 


FiG.  51. — Positive  or  ventricular  type  of  venous  pulse  in  tricuspid  insuflSciency,  showing  absence  of  the 
a  wave.     VJD,  right  jugular  vein;  ACS,  left  carotid  artery. 


JUG 


BRACK 


nomenon  is  readily  demonstrable  in  animals  (v.  Frey  and  Krehl)  and  need 
not  be  accompanied  by  any  change  in  heart-rate,  though  arrhythmia  is  fre- 
quently present  in  man.  In  animals  auricular  paralysis  or  marked  weaken- 
ing of  the  auricular  contraction  may  also  occur  as  the  result  of  vagus  stimu- 
lation, so  that  the  presence  of 
this  phenomenon  alone  is  not 
always  a  bad  omen,  though 
usually  such  is  the  case. 

Positive  Venous  Pulse. — 
When  the  auricle  is  paralyzed 
or  there  is  a  leak  at  the  tricuspid 
valve,  the  entire  form  of  the 
pulse-wave  usually  changes. 
The  collapse  during  ventricular 
systole  disappears  and  is  replaced 
by  a  systolic  plateau,  or  more 
usually  an  M-shaped  wave  with 
an  early  systolic  wave  c  or  p,  a 
midsystolic  depression,  and  a 
telesystolic  wave  v  (Hewlett). 
Mackenzie  believes  that  the 
first  crest  of  the  M  represents  a 

contraction  of  the  auricle  simultaneous  with  that  of  the  ventricle,  and 
that  the  depression  in  the  middle  corresponds  to  diastole  of  the  auricle; 
but  this  form  of  curve  has  been  obtained  by  Knoll  and  Theopold  in 
animals  when  the  auricles  were  stopped  by  vagus  inhibition.  This  form 
is  known  as  the  "positive,"  "ventricular,"  or,  from  the  fact  that  it 
appears  to  the  eye  as  a  single  wave,  the  "single"  type  of  venous  pulse 
(see  chapter  on  Tricuspid  Insufficiency).  Though  the  ventricular  type  of 
venous  pulse  occurs  in  tricuspid  insufficiency,  it  is  not  pathognomonic  of 
the  latter  and  may  indicate  merely  paralysis  of  the  auricle. 


Fig.  52. — Positive  or  ventricular  type  of  venous  pulse 
in  tricuspid  insufficiency,  showing  absence  of  the  a  wave. 
JUG,  right  jugular  vein;  BRACH,  right  brachial  artery. 


58 


DISEASES   OF   THE    HEART    AND    AORTA. 


Information  furnished  by  the  Venous  Pulse. — It  is  apparent  from  the 
above  deacription  that  the  following  facts  are  to  be  learned  from  the  normal 
venous  pulse-curve:  (1)  whether  the  auricle  (atrium)  is  contracting,  and 
whether  each  auricular  (atrial)  contraction  is  followed  by  a  ventricular  con- 
traction; (2)  the  time  required  for  the  conduction  of  the  impulse  from 
auricle  (atrium)  to  ventricle  (the  interval  a-c  on  the  tracing,  about  i  second 
in  normal  individuals — conduction  time) ;  (3)  whether  or  not  the  tricuspid 
valve  is  closing  perfectly  (shown  by  the  fall  of  pressure  during  systole 
and  the  subsequent  v  wave).^  In  irregular  pulses  many  more  important 
facts  are  to  be  learned  from  the  venous  pulses,  which  will  be  discussed  in 
connection  with  this  disturbance  of  function. 


(ESOPHAGEAL  TRACINGS. 

The  venous  pulse  tracing  reveals  the  conditions  prevaiUng  in  the  right  auricle  (atrium) 
and  the  state  of  the  tricuspid  valve.     A  corresponding  investigation  of  the  state  of  the 

left  auricle  (atrium)  and  of  the  mitral  valve 
Avas  made  possible  by  a  method  used  by 
Fredericq  in  animals  and  introduced  into 
clinical  medicine  by  Minkowski.  Minkowski 
calls  attention  to  the  fact  that  at  the  level  of 
the  seventh  to  the  ninth  thoracic  vertebrae 
(about  35  to  37  cm.  from  the  teeth)  the  left 
auricle  is  in  contact  with  the  oesophagus,  and 
when  one  introduces  a  stomach-tube  to  this 
level  it  receives  impulses  from  the  left  auricle 
I  f  /^(j^^l  I     alone.    Accordingly,  an  ordinary  stomach-tube 

B  n  I  /nriy|Lj»/  I     is  capped  with  a  thin  rubber  finger  cot,  and 

'  *  '  ^s»**»/  '     the  latter  secured  by  winding  a  silk  ligature 

several  times  around  it.     The  stomach-tube  is 
"IT  ~[1  l^^^*^/  \     then  swallowed  by  the  patient  until  it  extends 

'       ' '     "^ —  ^1  down  35  to  37  cm.  from  the  teeth.     It  is  then 

connected  with  a  Marey  tambour  whose  oscil- 
lations record  the  contraction  of  the  auricle 
and  ventricle  (Figs.  53  and  54).    The  fall  in 
the  wave  occurs  when  the  auricle  moves  away 
from    the    oesophagus,    the    rise    when    it    is 
pressed   against   the   latter   by  filling  with   blood.     Under  ordinary   circumstances   ven- 
tricular as  well  as  auricular  systole  draws  the  auricle  away  from  the  oesophagus  so 
that  the  falls  and   rises  correspond  to  auricular   and  ventricular  systole  respectively. 

CEsophageal  Tracing  in  Mitral 
Insufficiency. — When  the  mitral  valve 
does  not  close  (mitral  insufficiency), 
blood  is  forced  back  into  the  auricle 
during  ventricular  systole,  and,  instead 
of  a  fall,  there  is  a  rise  during  systole. 
Minkowski's  method  furnishes  the 
means  for  obtaining  the  missing  link 
in  our  knowledge  of  the  cardiac  impulse 
and  the  meaning  of  functional  murmurs, 
but  unfortunately  the  swallowing  of  the 

stomach-tube  is  so  disagreeable  to  the  ordinary  patient  and  so  dangerous  in  all  very 
severe  cases  as  to  preclude  its  adoption  into  general  use.  Patients  can,  however,  often 
be  trained  to  swallow  the  stomach-tube  without  difficulty,  or  a  rubber  tube  of  small  bore 
may  be  substituted,  and  then  very  satisfactory  results  may  be  obtained. 


Fig.  53. — Method  of  taking  tracing  from 
the  CEsophagus  to  show  the  contractions  of 
the  left  auricle.  The  arrow  points  to  the  thin 
rubber  bulb  at  the  end  of  the  oesophageal  tube. 
ST.,  stomach. 


CAROT. 


(ESOPH. 


Fig.  54.  —  (Esophageal   and    carotid    tracings  from   a 
nornaal  man. 


This,  as  has  been  shown  by  Mackenzie  and  by  Rihl,  is  not  absolute. 


THE   VENOUS  PULSE   AND  ELECTROCARDIOGRAM. 


59 


GAlVmOMLTLR 


LIFT 


RIGHT 


Fig.  55. — Simplest  form  of  apparatus  for  recording  the  electrocardiogram  and  cardiogram  simultaneously. 
LEFT  RIGHT,  jars  filled  with  salt  solution  to  receive  the  left  and  right  hands  respectively. 


Fig.  56.  —  Patient  with  both  hands  placed  in 
gars  of  salt  solution,  ready  for  taking  electrocardio- 
gram.    (After  Einthoven.) 


Fig.  57. — Course  of  the  electrical  variations  due 
to  the  heart-beat  in  man.  (After  Waller.)  c-c,course 
of  the  negative  wave  from  auricles  to  ventricles;  b,  b, 
zones  about  the  auricle  becoming  negative  during 
the  auricular  systole;  a,  a,  zones  about  the  ventricles 
becoming  negative  during  ventricular  systole. 


TTJift^^^^^B 


Fig.  58. — Normal  electrocardiogram  showing 
the  time  relations  to  the  venous  and  carotid  pulse- 
waves.     (After  Einthoven.) 


Fig.  59. — Normal  electrocardiogram  tracing 
taken  by  the  writer  in  collaboration  with  Prof. 
L.  F.  Barker  and  Dr.  G.  S.  Bond. 


60  DISEASES   OF   THE    HEART    AND    AORTA. 


INTRANASAL  TRACINGS. 

Mosso  and  also  the  writer  have  obtained  very  satisfactory  cardiographic  curves  from 
the  changes  of  air  pressure  within  the  thorax.  These  may  be  obtained  by  placing  in  one 
nostril  a  cork  perforated  by  a  glass  tube  which  is  connected  with  the  recording  lever.  The 
lips  are  closed  and  the  other  nostril  is  closed  by  pressure.  Or,  the  tube  may  be  placed 
in  the  mouth  and  both  nostrils  closed  by  pressure.  The  glottis  must  be  open  and  the 
breath  held.  Curves  thus  obtained  closely  resemble  the  oesophageal  tracings  in  normal 
individuals,  though  the  waves  are  smaller. 

THE   ELECTROCARDIOGRAM. 

Another  very  promising  method  of  examination  which  has  not  yet 
become  general  is  the  use  of  the  electrical  variations  due  to  the  heart  con- 
traction (electrocardiagram  of  Einthoven). 

Einthoven  places  the  patient  in  a  chair  with  both  hands  or  one  hand  and  one  foot 
inunersed  in  a  jar  of  0.9  per  cent,  sodium  chloride  solution.  Each  jar  is  connected  in  the 
circuit  with  a  very  delicate  Einthoven  (or  Edelmann)  thread  galvanometer  (Fig.  55). 
The  movements  of  the  galvanometer  are  recorded  photographically.  At  each  heart  con- 
traction a  series  of  electrical  changes  appear  (Figs.  58  and  59),  in  which  the  first  wave 
P  corresponds  to  the  auricular  (atrial),  the  second  QR  and  third  ST  to  the  ventricular 
systole.  This  method,  at  first  sight  the  most  difficult,  is,  when  the  appliances  are  once  set 
up,  one  of  the  simplest  of  all  the  graphic  methods.  Einthoven  has  connected  the  Leyden 
physiological  laboratory  with  the  hospital  by  means  of  telephone  wires  specially  laid,  and 
is  able  to  make  his  diagnoses  at  a  distance  of  a  mile  without  ever  seeing  the  patient. 

In  hypertrophy  of  the  right  ventricle  the  wave  QR  is  much  larger  than  usual  and  is 
en  the  same  side  of  the  base-line  as  the  auricular  wave  P.  In  cases  of  hypertrophy  of 
the  left  ventricle  the  QR  wave  is  inverted  and  its  altitude  is  also  greater  than  normal. 

Einthoven  and  Kraus  and  Nikolai  have  shown  that  extrasystoles  and  other  irregular- 
ities may  be  deciphered  by  this  method  better  than  by  means  of  the  venous  pulse;  and  it 
is  probable  that  it  will  to  a  great  measure  supplant  the  latter  as  a  means  of  diagnosis. 

BIBLIOGRAPHY. 
Venous  Pulse. 

Engelmann,  Th.  W.:  Ueber  den  Ursprung  der  Herzbewegungen,  Arch.  f.  d.  ges.  Physiol., 

Bonn,  1897,  Ixv,  109. 
Morrow,  W.  S.:  Ueber  die  Fortpflanzungsgeschwindigket  des  Venenpuls,  Arch.  f.  d.  ges. 

Physiol.,  Bonn,  1900,  Ixxix,  442.     The  Rate  of  Propagation  of  the  Venous  Pulse, 

Canad.  Rec.  Sc.,  1900,  viii,  205. 
Friedreich,  N.:  Ueber  den  Venenpuls,  Deutsch.  Arch.  f.  klin.  Med.,  Leipz.,  1865,  i,  241. 
Marey,  E.  J.:  La  circulation  du  sang  a  I'^tat  physiologique  et  dans  les  maladies,  Paris,  1881. 
Mackenzie,  J.:    The  Venous  and  Liver  Pulses,  and  the  Arrhythmic  Contraction  of  the 

Cardiac  Cavities,  Jour.  Path,  and  Bacteriol.,  Edinb.  and  Lond.,  1893-94,  ii,  pp.  84 

and  273.    The  Study  of  the  Pulse  and  Movements  of  the  Heart,  London,  1903. 
Hirschfelder,  A.  D.:  Graphic  Methods  in  the  Study  of  Cardiac  Diseases,  Am.  Jour.  M. 

Sc.,  Phila.,  1906,  cxxxii,  378. 
Bachman,  G.:  The  Interpretation  of  the  Venous  Pulse,  ibid.,  1908,  cxxxvi,  674. 
Hay,  J.:  Graphic  Methods  in  the  Study  of  Heart  Disease,  Oxford  and  Lond.,  1909. 
V.  Jaquet:  Cardiosphygmograph,  Ztschr.  f.  Biol.,  Muenchen,  1901. 
Mackenzie,  J.:  Diseases  of  the  Heart,  Oxford  and  Lond.,  1908. 
Uskoff,  L.:  Der  Sphygmotonograph,  Ztschr.  f.  klin.  Med.,  Berl.,  1908,  Ixvi,  90. 
Fredericq,  L.:    La  seconde  ondulation  positive  (premiere  ondulation  systolique)  du  pouls 

veineux  physiologique  chez  le  chien,  Arch,  intern,  de  Physiol.,   1907.     Historisch- 

kritische  Bemerkungen  ueber  die  von  klinischer  Seite  neuerdings  anerkannte  Identi- 

tat  der  Venen-  und  ffisophaguspulsbilder  mit  den  Vorkammerdruckkurven,  Zentralbl. 

f.  Physiol.,  I.eipz.  u.  Wien,  1908,  xxii,  297. 


THE  VENOUS   PULSE   AND   ELECTROCARDIOGRAM.        61 

Morrow,  W.  S.:  Various  Forms  of  the  Negative  or  Physiological  Venous  Pulse,  Brit.  M. 

Jour.,  Lond.,  1906,  ii,  1807.    The  Venous  Pulse,  ibid.,  1907,  i,  777. 
Knoll,  P.:  Beitrage  zur  Lehre  von  der  Blutbewegung  in  den  Venen,  Arch.  f.  d.  ges.  Physiol., 

Bonn,  1898,  Ixxii,  317,  621. 
Theopold,  P.:  Ein  Beitrag  zur  Lehre  von   der  Arhythniia  perpetua,  Deutsch.  Arch.  f. 

klin.  Med.,  Leipz.,  1905,  Ixxxii,  495. 
Marey,  E.  J.:  La  physiologie  du  sang  a  I'etat  physiologique  et  dans  les  maladies,  Paris,  1881. 
Fredericq,  L.,  1.  c. 

Porter,  W.  T.:  Researches  on  the  Filling  of  the  Heart,  Jour.  Physiol.,  Cam.,  1892,  xiii,  513. 
Bard,  L.:  Des  divers  details  du  pouls  veineux  les  jugulaires  chez  I'homme,  J.  de  Physiol. 

et  de  Path,  gen.,  Par.,  1906,  viii,  454. 
Hirschf elder,  A.  D.:  Some  Variations  in  the  Form  of  the  Venous  Pulse,  Bull.  Johns  Hop- 
kins Hosp.,  Bait.,  1907,  xviii,  265. 
Cushny,  A.  R.,  and  Grosh,  L.  C.-:  The  Venous  Pulse,  Jour.  Am.  M.  Ass.,  Chicago,  1907, 

xlix,  1254. 
Mackenzie,  J.:  The  Venous  Pulse,  Brit.  M.  J.,  Lond.,  1907,  i,  112. 
Sewall,  H.,  and  Hirschfelder,  A.  D.:  Unpublished  investigations. 
Peabody,  F.  W.:  Personal  communication. 
Sewall,  H.:    Safeguards  of  the  Heart-beat,  Am.  J.  M.  Sci.,  Phila.  and  N.  York,  1908, 

cxxxvi,  32. 
Hering,  H.  E. :    Die  Verzeichnung  des  Venepulses  am  isolierten  Kiinstlich  durchstromten 

Saugetierherzin,  Arch.  f.  d.  ges.  Physiol.,  Bonn,  1904,  cvi,  1. 
Chauveau  and  Marey:  Quoted  from  Marey,  La  Circulation  du  Sang,  etc. 
Gibson,  A.  G.:  On  a  Hitherto  Undescribed  Wave  in  the  Venous  Pulse,  Lancet,  Lond.,  1907, 

ii,  1380. 
Mackenzie,  J.:  The  Interpretation  of  the  Pulsations  in  the  Jugular  Veins,  Am.  Jour.  M. 

Sc,  Phila.  and  N.  York,  1907,  n.  s.  cxxxiv.  12. 
Rihl,  J.:  Ueber  den  Venenpuls  nach  experimenteller  Lasion  der  Trikuspidalklappe,  Ver- 

handl.  d.  Kong.  f.  innere  Med.,  Wiesbaden,  1907,  xxiv,  453. 
Gibson,  G.  A.:  Certain  Clinical  Features  of  Cardiac  Disease,  Johns  Hopkins  Hosp.  Bull., 

Bait.,  1908,  xix,  361. 
Eyster,  J.  A.  E. :  Unpublished  observations. 
Hirschfelder,  A.  D.:  Inspection  of  the  Jugular  Vein;    Its  Value  and  Its  Limitations  in 

Functional  Diagnosis,  J.  Am.  M.  Assoc,  Chicago,  1907,  xlviii,  1105. 
V.  Frev,  M.,  and  Krehl,  L.:  Untersuchungen  ueber  den  Puis,  Arch.  f.  Physiol.,  Leipz., 

1890,  31. 
Hewlett,  A.  W.:  On  the  Interpretation  of  the  Positive  Venous  Pulse,  Jour.  Med.  Re- 
search, Bost.,  1907,  xvii,  19. 
Minkowski,  O.:  Die  Registrierung  der  Herzbewegungen  am  linken  Vorhof,  Deutsch.  med. 

Wochnschr.,    1906,   xxxii,    1248.     Zur  Deutung  von   Herzarrhythmien  mittelst  des 

CEsophagealen  Kardiograms,  Ztschr.  f.  klin.  Med.,  Berl.,  1907,  Ixii,  371. 
Rautenberg,  E.:  Neue  Methode  der  Registrierung  der  Vorhofspulsation  vom  Oesophagus 

aus,  Deutsche  med.  Wchnschr.,  Leipz.  and  Berl.,  1907,  xxxiii,  364. 
Young,  C.  I.,  and  Hewlett,  A.  W.:  The  Normal  Pulsations  within  the  Oesophagus,  J.  M. 

Research.,  Bost.,   1907,  xvi,  427. 
Hirschfelder,  A.  D.:  Observations  on  a  Case  of  Palpitation  of  the  Heart,  Johns  Hopkins 

Hosp.  Bull.,  Baltimore,  1906,  xvii,  299. 
Einthoven,  W.:  Le  telecardiogramme,  Arch,  internat.  de  Physiol.,  Liege,  1906,  iv,  132. 

Weiteres  ueber  das  Elektrokardiogramm,  Arch.  f.  d.  ges.  Physiol.,  Bonn,  1908,  cxxii, 

517.    (See  also  chapter  on  Alterations  of  Rhythm.) 

ANALYSIS  OF  ALTERATIONS  IN  CARDIAC  RHYTHM. 

The  irregularities  in  rhythm  of  the  heart  may  be  divided  first  into 
three  classes:  (1)  arrhythmias,  in  which  there  is  no  discernible  order 
in  the  occurrence  of  beats;  (2)  allorrhy thmias  (altered  rhythms),  in 
which,  though  the  rhythm  is  not  regular,  yet  the  irregular  beats  occur 
according  to  a  certain  regular  system,  so  that  the  arrangement  of  these 


62  DISEASES   OF   THE   HEART   AND    AORTA. 

beats  in  one  section  of  the  tracing  can  be  prophesied  from  a  knowledge  of 
another ;  and  (3)  pararrhythmias  (Wenckebach) ,  in  which  two  separate 
rhythms  are  going  on  in  either  the  same  chamber  or  in  different  chambers 
at  the  same  time. 

ALLORRHYTHMIAS. 

A.  Of    extracardiac    origin. 

I.  Neurogenic,    due  to  more  or  less  rhythmic  reflex  stimuli  pass- 

ing through  the  vagi  and  accelerators  (toxic,  reflex  from  various 

organs,  respiratory  reflexes  from  lungs). 
a.  Associated  with  the  phases  of  respiration. 
6.  Not  associated  with  respiration — Mackenzie's  youthful  type. 

II.  Due    to    disturbances   in    the    filling    and    emptying 

of  the  heart  from  traction  upon  the  heart  and 
great  vessels — dropping  of  beats  without  heart-block,  pul- 
sus paradoxus  and  Riegel's  pulse. 

B.  Of    intracardiac    origin. 

I.  Due   to   disturbance   in    the   conduction    of    normal 
impulse  s — dropping  of  beats. 

1.  Auriculo-  (atrio-)  ventricular  block. 

2.  Sino-auricular  block. 

3.  Interventricular  (?)  block  (hemi systole). 

II.  Disturbance    of   contractilit  y — pulsus   alternans,   and 

failure  to  open  the  aortic  valves. 

III.  Occurrence    of    beats    in    response    to    abnormal 

stimuli    or    increased    irritability. 

1.  Extrasystoles,  in  which  irregular  beat  is  brought  on  by  a  single  abnormal 

stimulus. 
a.  Ventricular. 
h.  Auricular, 
c.  Auriculo-  (atrio-)   ventricular. 

2.  Permanently  irregular  heart. 

3.  Paroxysmal  tachycardia  (auricular  fibrillation). 

I.    NEUROGENIC     .\LLORRHYTHMIAS. 

Alteration  in  cardiac  rhythm  resulting  from  intermittent  stimuh 
passing  down  the  cardiac  nerves  constitutes  one  of  the  most  common  forms 
of  cardiac  allorrhythmias.  As  has  been  seen  (Chapter  III.),  altera- 
tions of  the  pulse-rate  may  result  from  any  stimu- 
lation of  .any  afferent  nerve,  from  skin,  muscles,  mucous 
membrane,  and  viscera,  or  from  stimuh  arising  in  the  vagal  or  accelerator 
centres  in  the  medulla. 

As  Reid  Hunt  and  Hooker  have  shown,  the  reflex  stimulation  may  cause  a  slowing 
of  the  pulse-rate  through  stimulation  of  the  vagus  centre,  or,  under  other  circumstance- 
and  especially  when  of  a  different  intensity,  it  may  cause  an  acceleration  of  the  pulses 
rate.  Hunt  has  shown  that  this  acceleration  is  due  chiefly  to  momentary  cessation  of  the 
tonic  stimuli  in  the  vagus;  but  Hooker  proves  that  there  is  also  a  stimulation  of  the 
accelerators.  Such  afferent  or  sensory  stimuli  may  arise  in  the  skin  and  muscles,  but 
especially  in  the  viscera  and  the  serous  and  mucous  membranes. 


THE  VENOUS   PULSE    AND   ELECTROCARDIOGRAM.        63 


Respiratory 
allorrhythmia 


AURICCLO- 
VENTRICULAR 
HEART-BLOCK 


Paroxysmal 
tachycardia 


Fig.  60. — Diagram  representing  various  types  of  irregular  pulse.  The  heavy  white  arrows  indi- 
cate the  site  of  origin  of  the  disturbance  of  rhythm.  The  heavy  white  lines  indicate  the  course  of  the 
abnormal  cardiac  impulses.  RESP,  respiration;  AUR,  auricle;  A-V  or  AVB  auriculoventricular  bun- 
dle; VENT,  ventricle;  CAR,  carotid  pulse;  VEN,  venous  pulse;  SIN,  sinus  region  of  the  heart;  SVC, 
IVC,  superior  and  inferior  venae  cava",  respectively. 


Reflex  Allorrhythmias. — Fran^ois-Franck  and  KobLanck  and  Roeder 
have  been  able  to  produce  such  an  arrhythmia  by  stimulating  the  mucous 
membrane  of  the  nasal  septum  at  a  point  just  opposite  the  middle  turbinate 
bone,  and  Stadler  and  Hirsch  have  done  so  by  stimulating  the  walls  of 
the  stomach  and  intestines.    There  is  normally  a  reflex  slowing  of  the  heart 


64 


DISEASES   OF   THE   HEART   AND    AORTA. 


during  swallowing,  and  similar  periodic  slowing  of  the  rate  from  stimulations 
of  the  vagus  may  account  for  many  of  the  disturbances  of  rhythm  in  air- 
swallowxrs.  Moreover,  Einthoven  has  shown,  by  recording  the  electrical 
variations  in  the  peripheral  stump  of  the  divided  vagus,  that,  with  each 
inspiration,  afferent  stimuli  are  passing  up  the  vagus,  and  these  may  evoke 
reflex  responses  when  the  entire  nervous  system  is  abnormally  sensitive. 

Occurrence.  —  Neurogenic  arrhythmias  are  particularly  common  in 
children  and  in  young  persons,  and  hence  are  designated  by  Mackenzie 
as  the  "youthful  type,"  but  this  is  only  because  the  cardiac,  vaso- 
motor, and  respiratory  centres  are  in.  more  labile  equilibrium  in  them  than 
in  normal  adults.  However,  whenever  the  nervous  system  becomes  more 
irritable, — from  the  occurrence  of  visceral  reflexes,  emotions,  or  toxic 
influences  (bacterial  toxins,  alcohol,  tobacco,  coffee,  etc.), —  stimuli  (like 
those  passing  up  the  vagus)  which  are  normally  subminimal  become 
effective.  Hence  allorrhythmias  of  this  type  arise  in  nervous  individuals 
and  in  the  so-called  functional  cardiac  diseases  or  cardiac  neuroses  (Part  IV, 
Chapter  III).  Since  the  afferent  stimuli  in  the  vagus  are  continually  act- 
ing, it  is  quite  natural  that  they  should  add  themselves  to  any  other  afferent 


RESPIRATION 


RADIAL 


Fig.  61. — Respiratory  arrhythmia.     (After  Hewlett.) 


stimuli  which  may  also  be  acting,  and  that  the  alterations  of  rhythm  will 
then  be  associated  with  respiration;  and,  since  the  nature  of  reflex 
responses  varies  with  slight  variations  in  the  intensity  of  the  stimulus, 
it  is  not  surprising  that  there  is  in  some  cases  a  series  of  slow  beats 
associated  with  inspiration  and  a  series  of  rapid  beats  in  expiration  (Fig. 
54),  while  in  others  the  slowing  occurs  during  expiration  and  the  rapid 
beats  are  during  inspiration.  This  latter  type  is  often  spoken  of  as  normal, 
but  in  perfectly  normal  individuals  the  rate  may  be  absolutely  regular. 

Reissner  has  shown  that  the  irregularity  is  sometimes  of  psychic 
origin;  or,  in  other  words,  that  the  stimulus  exciting  the  cardiac  nerves 
may  descend  from  the  cerebral  cortex  instead  of  ascending  by  the  usual 
paths  of  afferent  stimuli.  This  psychogenic  arrhythmia  is  not  extremely 
uncommon.  Indeed,  the  writer,  whose  pulse  has  been  regular  at  all  other 
times,  experienced  such  an  irregularity  upon  one  occasion  of  intense  anxiety 
lasting  for  several  minutes.  The  pulse  became  regular  as  soon  as  the 
anxiety  passed  off;  and  has  remained  so  for  five  3'ears,  in  spite  of  a  severe 
tonsillitis  and  tonsillectomy. 

As  Reyfisch  has  shown,  similar  neurogenic  allorrhythmias  occur  in 
meningitis  and  in  conditions  with  increased  intracranial  ten- 
sion and,  as  Eyster  has  shown,  in  association  with  Cheyne-Stokes  breath- 
ing. Mackenzie  has  also  shown  that  there  are  many  other  cases  in  which 
neurogenic  irregularity  is  not  associated  with  the  phases  of  respiration.    In 


THE   VENOUS   PULSE    AND   ELECTROCARDIOGRAM.         65 

these  it  may  be  either  periodic  or  entirely  intermittent.  It  is  most  important 
that  the  exact  mode  of  origin  of  such  stimuU  and  its  characteristics  should 
be  carefully  studied,  since  this  arrhythmia  must  be  differenti- 
ated from  those  of  myocardial  origin.  In  these  cases,  though 
the  relation  of  the  allorrhythmia  to  respiration  may  be  timed  by  palpation 
and  inspection,  a  careful  venous  tracing  should  be  made  lest  an  extra- 
systolic  irregularity  be  diagnosed  when  it  does  not  actually  exist. 

Characteristics  of  Reflex  Allorrhythmias.  —  The  striking  feature  of 
these  neurogenic  disturbances  of  rhythm  is  that  they  are  often  charac- 
terized by  instability  of  rhythm,  by  the  occurrence  of  rhythmic 
changes  in  rate  rather  than  by  the  interpolation  of  beats  which  differ  from 
the  others  in  character.  The  beats  usually  occur  in  short  groups,  the  first 
beat  of  the  slower  group  being  the  longest,  the  rate  of  the  more  rapid  series 
showing  a  progressive  increase.  The  last  beat  of  the  rapid  series,  with 
the  vagal  pause  following  it,  may  be  mistaken  for  an  extrasystole ;  but,  on 
examining  the  few  beats  preceding,  it  will  be  seen  that  this  beat  was  not 
premature  and  not  due  to  an  abnormal  stimulus.  Moreover,  the  beats 
are  usually  of  full  and  almost  equal  strength,  thereby  differing  from 
the  feeble  beats  of  extrasystoles;  and  they  do  not  occur,  as  do  the  latter, 
abnormally  early  in  the  cardiac  cycle.  It  is  an  irregularity  in  rhythm  rather 
than  an  irregularity  in  force,  though  a  certain  degree  of  the  latter  may  be 
present  through  the  action  of  the  vagus  on  the  heart. 

The  rhythm  usually  becomes  regular  within  half  an  hour  after  the 
hypodermic  administration  of  atropine,  .0005  to  .001  Gm.  (y^o  to  oV  gr-)- 
This  rule  is  not  invariable. 

When  long  pauses  alternate  with  short  series  of  rapid  beats,  the  force 
of  the  first  large  beat  may  be  slightly  below  that  of  the  smaller  beats,  as 
shown  by  tracings  with  the  Erlanger  apparatus  at  or  near  the  maximal 
pressure.  With  extrasystoles  the  systolic  pressure  of  the  smaller  beats  is 
usually  less  than  that  of  the  regular  (large)  beat.  In  both  cases,  however, 
this  depends  upon  too  many  factors  (time  at  which  the  extrasystole  occurs, 
amount  of  systolic  output,  amount  of  peripheral  resistance,  factors  causing 
the  extrasystole,  etc.)  to  be  regarded  as  absolute  criterion  for  diagnosis. 

II.  Respiratory  (Pulsus  paradoxus  and  Riegel's  Pulse). — As  will  be 
seen  in  the  chapters  on  adherent  pericardium  (page  506)  and  enterop- 
tosis,  traction  upon  the  aorta  during  respiration  may  prevent  the  heart 
from  emptying  itself  and  thus  cause  the  dropping  of  a  beat  in  the  arteries. 
Or,  on  the  other  hand,  traction  upon  the  great  veins  may  produce  the  same 
effect  by  preventing  the  heart  from  filling.  When  there  are  adhesions  in 
the  posterior  mediastinum  or  when  the  diaphragm  is  low,  this  dropping 
occurs  during  inspiration  (pulsus  paradoxus,  Kussmaul),  whereas  when 
there  are  adhesions  between  the  heart  and  the  anterior  chest  wall  it  may 
occur  in  expiration  (Riegel). 

ALLORRHYTHMIAS    HAVING    THEIR     ORIGIN    WITHIN    THE    HEART. 

III.  Allorrhythmias  due  to  Failure  to  Conduct  Impulses  generated 
Normally — Heart=block.' — Of  this  there  are  several  tj-pes.     (1)  A  u  r  i  c  u  1  o  - 

'  A  full  discussion  may  be  found  in  Part  III,  Chapter  XI. 


66 


DISEASES    OF   THE   HEART   AND    AORTA. 


ventricular  Heart-block. — The  more  usual,  or  at  least  better  known, 
type  of  blocking  the  impulses  is  at  the  auriculoventricular  junction.  In 
this  type  no  change  occurs  in  the  origination  of  the  cardiac  impulse  or  in 
the  contraction  of  the  auricles  (atria),  but  the  conductivity  of  the  impulse 
to  the  ventricle  by  the  bundle  of  His  is  impaired.  Such  impairment  may  be 
(a)  functional,  from  overstimulation  of  the  vagus,  of  which  frequent 


A  SEC. 


JUG. 


APEX 


^AMJ^juLMju^^^ij^^h 


BRACH. 


A  /\.A 


P^essUHB     0/\l      VA<iUS 


Fig.  62. — Venous  tracings  in  heart-block.     Partial  heart-block    (3  : 1  rhythm)  during  pressure  on  the 
vagus,  in  a  case  of  Adams-Stokes  disease. 

examples  are  seen  in  every  laboratory  experiment.  Clinically  this  may  be 
seen  also  in  the  cases  of  digitalis  poisoning  and  postfebrile  bradycardia, 
especially  after  pneumonia  and  influenza,  occasionally  also  in  cases  in  which 
there  is  a  tumor  pressing  upon  the  vagus.  (6)  Organic,  from  interrup- 
tion of  the  bundle  of  His.  In  this  case  the  block  may  be  increased  by  giving 
atropine  or  anything  else  that  quickens  the  heart,  or  it  may  not  be  affected. 


Fig.  68. — Venous  tracings  in  heart-block.     Complete  heart-block  in  a  case  of  Adams-Stokes  disease. 

(c)  There  may  be  a  combination  of  the  two  effects  (v.  Tabora, 
Gibson,  Thayer) ,  the  conductivity  of  the  injured  Purkinje  fibres  of  the  bundle 
being  still  further  diminished  by  the  action  of  the  vagus  upon  them,  and 
this  effect  outweighing  the  favorable  action  in  slowing  the  auricular  rhythm. 
The  block  may  be  partial  or  complete,  depending  upon  whether 
the  ventricles  still  follow  the  lead  of  the  auricles  or  initiate  their  own  rhythm. 
Thus,  in  the  partial  block  the  ventricles  may  respond  to  only  every  second, 
third,  or  fourth,  or  even  only  every  sixteenth  contraction,  or  may  sometimes 


THE   VENOUS   PULSE   AND   ELECTROCARDIOGRAM.        67 

respond  to  every  second,  sometimes  to  every  fourth  beat,  etc.  On  the  other 
hand,  they  may  fail  to  contract  at  all  over  a  considerable  period  (stoppage) 
during  which  syncope  (Adams-Stokes  syndrome),  epileptiform  seizures, 
or  death  may  set  in  (Erlanger),  or,  after  a  stoppage  of  greater  or  less  dura- 
tion, they  may  begin  to  beat  at  a  rhythm  of  their  own,  bearing  no  relation 
at  all  to  the  rhythm  of  the  auricles  (complete  block).  This  constitutes  the 
permanent  bradycardia  of  Adams-Stokes  disease. 

(2)  Sino-auricular  Block. — Sino-auricular  block  may  also  occur,  the 
cardiac  impulse  being  generated  as  usual  at  the  mouths  of  the  great  veins 
and  coronary  sinus  in  the  region  homologous  with  the  sinus  venosus  of  the 
frog,  but  may  fail  to  be  communicated  to  the  auricles. 

Keith  and  Schonberg  have  shown  that  this  could  scarcely  be  the  result  of  a  localized 
lesion,  and  would  therefore  depend  upon  the  difference  in  the  properties  and  irritability 
of  auricular  and  venous  musculature  rather  than  organic  block.  The  presence  of  such 
blocks  is  assumed  by  August  Hoffmann  in  paroxysmal  tachycardia,  in  which  there  is 
a  sudden  doubling  or  even  quadrupling  of  the  pulse-rate  during  the  attacks,  and  by 
Hewlett  in  digitalis  poisoning.  Experimentally  they  have  been  produced  by  Erlanger 
and  Blackman  on  the  excised  mammalian  heart,  but  b.oth  Hirschfelder  and  Eyster  and 
the  former  observers  failed  to  do  so  in  the  heart  in  situ.  Gibson  assumes  the  existence  of 
a  similar  block  in  a  case  of  Adams-Stokes  disease,  which  he  cites,  along  with  the  block 
at  the  auriculoventricular  junction. 


APEX 


Fig.  64. — Occasional  absence  of  apex  impulse  during  inspiration  simulating  interventricular  heart-block. 

(3)  Interventricular  Block  (Hemisystole). — v.  Leyden  in  1868  reported 
a  case  of  bigeminal  pulse  in  which  he  assumed  that  one  ventricle  was  con- 
tracting without  the  other. 

This  case  and  other  cases  reported  by  the  older  writers,  and  which  were  undoubtedly 
due  to  extrasystoles,  are  really  not  conclusive;  but  recently  cases  have  been  reported  by 
Kraus  and  Nikolai,  and  by  Hewlett  and  Schmoll,  in  which  the  electrocardiogram  and 
venous  tracings  have  furnished  some  evidence  that  the  right  ventricle  and  the  left  ven- 
tricle may  have  been  contracting  alternately  and  not  synchronously.  For  the  present, 
one  is  justified  in  an  attitude  of  moderate  scepticism  upon  this  point  until  absolute  proof 
has  been  brought.  Professor  Barker,  Dr.  Bond,  and  the  writer  have  repeatedly  cut  through 
the  left  branch  of  the  His  bundle  without  injuring  the  right  branch.  No  asynchronism 
of  the  ventricles  occurred.  Extrasystoles  produced  in  either  ventricle  were  conducted 
to  the  other  without  delay.  It  does  not,  therefore,  seem  probable  that  a  patch  of  endo- 
carditis or  myocarditis,  such  as  Aschoff  and  Tawara  occasionally  found  invading  a  single 
branch  of  the  His  bundle,  would  be  able  to  block  the  impulse  to  one  ventricle  and  thereby 
prevent  its  contraction.  Moreover,  it  is  possible  that,  like  v.  Leyden's,  Hewlett's  tracings 
may  permit  of  a  different  and  more  conventional  explanation. 

IV.  Diminution  in  Contractile  Power — Pulsus  alternans. — When  the 
contractile  power  of  the  heart  diminishes,  or,  more  frequently,  when  the 
rate  is  increased  to  the  point  that  the  heart  has  some  difficulty  in  carry- 
ing out  effectual  contractions,  it  is  found  that  the  alternate  contractions 


68 


DISEASES   OF   THE    HEART   AND    AORTA. 


are  of  different  size,  some  larger,  some  smaller,  giving  rise  to  the  condition 
known  as  pulsus  alternans  or  alternating  pulse.  This  is  especially  common 
in  the  tachycardias  associated  with  some  weakness  of  the  heart  muscle, 


Fig.  65. — Alternating  pulse  in  a  case  of  paroxysmal  tachycardia. 

and  especially  with  paroxysmal  tachycardia;  but  wherever  it  occurs  it  is  an 
expression  of  disproportion  between  the  rate  and  contractility  of  the  heart 
(or,  in  Engelmann's  terminology,  between  the  chronotropic  and  ino- 
tropic   influences). 

Experimentally  this  can  be  readily  shown  by  throwing  induction  shocks  into  the 
heart  at  a  rate  which  it  can  barely  follow.  A  pulsus  alternans  invariably  results  (Hirsch- 
felder,  Hering).  After  a  few  seconds  or  minutes  the  heart  has  gained  its  full  contractility 
and  the  alternating  character  disappears,  only  to  reappear  when  it  begins  to  weaken. 
The  same  phenomenon  is  also  seen  in  attacks  of  paroxysmal  tachycardia  (Fig.  65).  Pul- 
sus alternans  is  also  present  in  some  cases  of  angina  pectoris  (Mackenzie).  It  then  indi- 
cates that  the  heart  is  in  a  weakened  condition. 

V.  Dropping  of  Beat  owing  to  too  low  Contractility. — If  the  auricle  be  stimulated 
directly  at  a  rate  still  more  rapid,  it  can  no  longer  follow  every  single  stimulus,  but  occa- 
sionally one  beat  is  dropped  out,  just  as  is  the  case  in  a  partial  heart-block,  although  the 

stimulus  is  being  applied  directly  to  the  auricle, 
which  intennits  a  little  more  rapidly,  and  it  fol- 
lows only  alternate  stimuli.  If  the  irritability  of 
the  auricle  be  now  suddenly  increased,  as  by 
|30uring  warm  salt  solution  over  it,  it  will  sud- 
denly respond  with  a  contraction  to  each  instead 
of  to  alternate  stimuli,  or  it  may  respond  occa- 
sionally to  all  and  occasionally  to  only  alternate 
stimuli,  giving  an  allorrhythmia  1:1  +  2:1. 
Thus  we  may  have  allorrhythmias  simulating 
partial  heart -blocks  on  the  one  hand,  and  extra- 
systoles  on  the  other,  due  merely  to  general 
decrease  in  the  irritability  of  the  entire  mus- 
culature without  any  special  disturbance  in 
conductivity:  and  just  such  inotrophic  and 
bathmotrophic  variations  may  be  responsible 
for  many  of  the  so-called  veno-auricular  heart- 
blocks,  such  as  have  been  described  by  Hewlett 
and  Wenckebach. 


EXTRASYSTOLES. 

Irregularities  may  be  due  to  the 
origination  of  abnormal  cardiac  im- 
pulses or  to  abnormal  response  to 
stimuli  (extrasystoles) .  The  simplest 
form  of  this  is  seen  in  the  occurrence 
of  single  abnormal  beats.  Experimentally  it  has  been  shown  (Marey) 
that  when  a  single  electrical  or  mechanical  stimulus  is  applied  to  the 
heart    at    any  time    except    the  refTactory  period,    the    latter    responds 


Fig.  66. — Response  of  frog's  ventricle  to 
abnormal  stimuli.  (After  Marey.)  Electric 
shock  thrown  into  it  at  the  instant  marked  by 
the  nick  in  the  base  line  and  by  the  dotted  line. 


THE  VENOUS  PULSE  AND  ELECTROCARDIOGRAM. 


69 


almost    immediately    with  a   contraction    (extras y stole,   Engelmann; 
premature    systole,   Mackenzie,  Cushny,  and  Matthews). 

Ventricular  Extrasystoles. — If  the  extra  stimulus  be  applied  to  the 
ventricle,  the  latter  responds  with  a  premature  contraction,  then  usually 
but  not  always  misses  the  next  impulse  from  the  auricle  and  pauses  for  a 


- — ivv 

V.J.D.  - 


3kc  ^^-'^ 


Fig.  67. — Tracing  from  the  jugular  vein  (1'.  J.  D.)  and  bracliial  artery  (.4.  B.  R.)  in  man,  showing 
ventricular  extrasystoles.    Time  markings  in  5  seconds.    E,  extrasystoles  arising  in  the  ventricle  (not  pre- 

3.0  +  5^^  2X4^ 
~       5     • 


ceded  by  an  a  wave).    Time  of  the  bigeminus  (regular  systole  +  extrasystole  +  pause) 


while,  until  the  second  impulse  from  the  auricle  reaches  it.  We  have,  there- 
fore, a  normal  contraction,  a  premature  contraction,  and  the  subsequent 
pause  (which  together  may  be  termed  a  bigeminus),  lasting  as  long  as 
two  regular  contractions.  The  bigeminus  may  be  spoken  of  as  a  "full 
bigeminus''  when  it  lasts  through  two  full  cardiac 
cycles,  and  a  "  s  h  o  r  t  e  n  e  d  bigeminus"  when  the  duration 
of  regular  systole  +  extras3'stolc  +  subsequent  pause 
is  less   than   two    cardiac    cycles. 

Auricular  Extrasystoles. — When,  however,  the  extra  stimulus  is  applied 
to  the  great  veins  or  the  auricle,  the  bigeminus  lasts  less  than  two  cardiac 
cycles  if  the  stimulus  follows  closely  upon  the  regular  contraction,  and 
exactly  equal  to  two  cycles  if  it  is  applied  late  (Hirschfelder  and  Eyster). 
If  the  stimulus  is  applied  early,  the  auriculoventricular  (atrioventricular) 
conduction  time  (a-c)  interval  is  slowed.    Later  in  the  cycle  it  is  unchanged. 


JUG. 


BRACK. 


Fig.  68. — Tracings  from  the  jugular  vein  and  brachial  artery  of  a  patient  with  trigeminal  pulse  due 
to  the  regular  occurrence  of  two  auricular  extrasystoles  (E,  E)  after  each  regular  systole.  The  a  wave 
and  general  form  of  the  venous  pulse  are  the  same  for  the  regular  and  the  auricular  extrasystoles. 


The  two  forms  of  extrasystoles  occur  clinically  and  may  be  differ- 
entiated by  the  analysis  of  the  venous  pulse;  the  extrasystoles  of  auricular 
(atrial)  origin  often  give  rise  to  shortened  bigemini,  while  ven- 
tricular extrasystoles  always  cause  full  bigemini.  In  the 
tracings  of  auricular  extrasystoles  one  can  see  the  auricular  wave  before 
the  ventricular  even  in  the  extrasystole;  the  ventricular  showing  a  single 
large  wave  due  to  ventricular  systole,  sometimes  with  the  notch  due  to 
the  contraction  of  the  auricle  from  reversed  conduction  of  the  impulse. 


70 


DISEASES   OF   THE   HEART    AND    AORTA. 


Occasionally  ventricular  extrasystolescan  be  distin- 
guished on  inspection  by  the  large  flapping  "single" 
pulsation   in   the   jugular   vein    which    accompanies    them,    in 

contrast  to  the  double  venous  pulse  of  the 
normal  beats  and  the  auricular  extra- 
systoles  (Hirschfelder) . 


RIGHT 


LEFT 


A  further  advance  in  the  cHnical  study  of 
extrasystoles  is  due  to  the  clinical  use  of  the  elec- 
trocardiogram by  Einthoven  and  his  pupils,  and  more 
recently  by  Kraus  and  Nikolai,  Hering,  and  Lewis. 
Einthoven  called  attention  to  the  presence  of 
certain  very  peculiarly  formed  electrocardiograms 
obtained  from  irregularly  acting  hearts.  Kraus  and 
Nikolai  were  able  to  reproduce  these  abnormal  waves 
by  producing  extrasystoles  in  dogs;  and  found  that 
extrasystoles  arising  in  the  right  and  left  ventri- 
cles respectively  produced  curves  which  were  the  inverse  of  one  another  (Fig.  69). 

Kahn  in  Hering's  laboratory  has  been  able  to  confirm  these  findings  in  great  part. 
However,  he  calls  attention  to  the  fact  that  they  do  not  hold  absolutely,  and  shows  that 
stimuli  applied  to  neighboring  points  in  right  and  left  ventricles,  near  the  apex,  may  elicit 
electrocardiograms  which  differ  only  slightly  from  one  another. 


Fio.  69. — Diagrammatic  reproduction 
of  the  electrocardiogram  obtained  in  the 
dog  as  the  result  of  extrasystoles  arising 
in  the  right  and  left  ventricles.  (After 
Kraus  and  Nikolai.) 


T     P 


R    T 


tXTKASY 


Fig.  70. — Electrocardiogram  of  a  patient  with  mitral  stenosis,  showing  extrasystoles,  wliich 
arise  in  the  right  side  of  the  heart.  Taken  by  the  writer  in  collaboration  with  Prof.  L.  F.  Barker  and 
Dr.  Ci.  S.  Bond.  Current  led  off  from  the  right  hand  and  left  foot.  Lettering  of  curves  as  in  Fig.  t9. 
P  R  T  represent  normal  waves;  EXTRASYS,  extrasystoles. 

Stimuli  which  Cause  Extrasystoles. — The  question  as  to  the  nature  of 
the  stimulus  which  gives  rise  to  extrasystoles  in  man  is  of  the  greatest 
practical  importance,  for  many  writers  (especially  Fr.  Miiller)  are  of  the 
belief  that  they  never  occur  unless  the  heart  muscle  is  diseased.  On  the 
other  hand,  Mackenzie,  whose  observations  have  been  extended  over  a 
period  of  fifteen  years,  regards  them  as  of  no  special  significance  either  in 
prognosis  or  in  influencing  the  patient's  manner  of  life.  He  mentions  hav- 
ing advised  one  of  his  patients  to  continue  playing  football  in  spite  of  his 
extrasystoles,  and  adds  that  the  extrasystoles  disappeared! 

Experimentally  it  has  been  shown  by  Knoll,  Marey,  Hering,  and  others  that  ventric- 
ular extrasystoles  may  be  produced  whenever  either  the  left  ventricle  or  the  right  is  pre- 
vented from  emptying  itself  (i.e.,  by  clamping  the  aorta  or  the  pulmonary  artery).  In 
man  they  are  also  most  common  in  conditions  in  which  there  is  a  high  blood-pressure  and 
the  heart  is  just  beginning  to  fail  (chronic  nephritis,  myocarditis,  aortic  insufficiency), 
and  probably  fails  to  discharge  a  sufficient  amount  of  its  contents.  This  probably  acts  as 
a  stimulus  for  a  second  extrasystole,  as  is  frequently  seen  (pulsus  trigeminus).  Ventricular 
extrasystoles  are  most  common  in  hearts  whose  rate  is  slow  and  hence  which  discharge 
^  large  amount  of  blood.    They  are  particularly  common  at  the  end  of  the  first  third  of 


THE   VENOUS   PULSE   AND   ELECTROCARDIOGRAM.        71 

diastole  when  the  filHng  of  the  ventricle  is  nearing  completion.  The  ventricular  fibres  are 
stretched  more  or  less  by  the  influx,  and  in  conditions  of  increased  irritability  the  stretch- 
ing of  the  fibres  may  act  as  a  stimulus  and  give  rise  to  the  extrasystoles. 

Similar  conditions  are  observed  with  reference  to  the  auricle.  Dr.  Cameron,  in  the 
writer's  laboratory,  observed  an  instance  of  permanent  bigeminal  pulse  in  a  dog  due  to 
the  presence  of  a   bubble   of  air  in   the   right   auricle.     The  air  had  entered 


VOLUME  OF 
VENTRICLES 


BLOOD-PRESSURE 


SECONDS 

Fig.  71. — Volume  curve  of  the  ventricles,  showing  the  dilatation  which  followed  the  entrance 
of  an  air-bubble  into  the  right  auricle.  (Kindness  of  Dr.  Cameron.)  The  extrasystoles  drive  very  little 
blood  into  the  aorta.    DIL,  dilatation. 

from  a  hypodermic  syringe  during  an  intravenous  injection.  When  the  bubble  was  mas- 
saged out  of  the  auricle  the  bigeminal  pulse  disappeared.  It  seems  not  improbable  that 
mural  thrombi  may  play  a  similar  role,  though  it  is  certain  that  this  is  not  always  the  case. 
Auricular  extrasystoles  may  also  be  produced  experimentally  by  causing  a  steno- 
sis at  the  auriculoventricular  orifices  (Hirschf elder).  Clinically  they  occur  quite  com- 
monly in  mitral  disease  and  most  frequently  begin  at  the  time  of  the  v  wave,  the  very 
instant  in  the  cycle  at  which  the  auricle  is  most  distended  j(Fig.  68).  Nevertheless,  it  must 
be  confessed  that  much  remains  to  be  learned  regarding  the  nature  of  the  stimulus  or 
stimuli,  and  the  actual  functional  significance  of  extrasystoles. 

Palpitation  with  Extrasystoles.  • —  Extrasystoles  are  very  frequently 
associated  clinically  with  cardiac  hyperaesthesia  in  the  form  of  palpitation, 
so  that  many  clinicians  erroneously  regard  all  irregularities  with  palpita- 
tion as  extrasystolic.  However,  it  is  possible  that  this  hypersensibility 
about  the  heart  may  have  some  causal  relation,  since  Hornung  has  shown 
that  extrasystoles  in  the  dog  are  most  readily  produced  by  stimulating  in 
the  vicinity  of  the  cardiac  nerves — auriculo(atrio)  ventricular  and  inter- 
ventricular grooves — and  that  they  cannot  be  produced  after  cocainizing 
the  epicardium.  True  extrasystoles  cannot  be  produced  experimentally  by 
stimulation  of  nerves  (Hoffmann,  Hering),  and  though  it  is  occasionally 
claimed  that  they  occur  in  gastro-intestinal  diseases  the  exact  relation  is 
not  clear.  It  is  certain  that  they  are  often  brought  on  by  constipation 
and  flatulence  in  certain  persons,  but  whether  there  is  a  myocardial  lesion 
already  present  in  these  cases  is  a  still  open  question. 

Diagnosis  of  Extrasystoles. — In  some  cases  it  is  very  difficult  to  dis- 
tinguish between  the  neurogenic  irregularities  and  the  auricular  extra- 
systoles. Dehio  has  called  attention  to  the  fact  that  the  former  disappear 
under  the  administration  of  atropine,  while  the  latter  remain  unaltered. 
Nevertheless  one  cannot  always  be  certain  that  the  dose  of  atropine,  even 
if  it  has  given  rise  to  symptoms,  has  been  large  enough  to  produce  the  effect. 


72  DISEASES   OF   THE   HEART   AND   AORTA. 

An  example  of  this  type  was  present  in  a  patient  seen  byithe  writer  several  years 
ago,  in  whom  palpitation  and  arrhythmia  had  been  present  for  several  years,  the  patient 
being  conscious  not  only  of  the  occcurrene  but  also  of  the  size  of  every  beat,  and  noticing 
especially  a  group  of  one  large  beat  with  two  small  ones  followed  by  a  pause  (pulsus  trigem- 
inus). The  tracing  made  while  the  patient  was  in  the  hospital  showed  that  these  were 
due  to  a  single  beat  followed  by  two  smaller  and  earlier  ones  and  then  by  a  pause,  all  the 
beats  being  preceded  by  an  auricular  contraction  (a  wave).  This  irregularity  was  much 
more  marked  whenever  the  patient  was  constipated,  but  it  also  persisted  after  0.5  mg. 
(t27t  gr)  atropine,  which  gave  the  patient  marked  symptoms  but  caused  no  change 
in  rate.  In  such  a  case  it  is  very  difficult  to  state  whether  we  have  to  deal  with  auricular 
extrasystoles  or  with  a  very  rapid  pulse  interrupted  by  variations  in  diastole  (youthful 
type).  The  ineffectiveness  of  atropine  and  the  extreme  irregularity  are  against  the  latter 
view.  However,  the  diagnosis  of  extrasystoles  can  usually  be  made  by  means  of  the 
electrocardiogram. 

In  the  routine  physical  examination  extrasystoles  may  often  be  diag- 
nosed on  auscultation  by  the  abrupt  change  from  a  rhythm  1-2  —  1-2 

—  1-2,  etc.,  to  1-2-3-4 1-2,  etc.    Accompanying  this  there  may 

be  seen  an  early  wave  in  the  jugular  pulse.  In  the  case  of  auricular  extra- 
systoles the  pulsation  does  not  differ  from  the  double  pulse  of  the  regular 
beat,  but  with  ventricular  extrasystoles  there  is  a  single  wave,  large, 
conspicuous,  and  flapping. 

Ineffectual  Contractions. — When  the  extrasystole  occurs  early  in  dia- 
stole, the  heart  may  not  have  recovered  from  the  effect  of  the  last  systole 
sufficiently  to  generate  a  forcible  contraction.  The  aortic  valves  are  not 
opened.     The  aortic  second  of  the  extrasystole  disappears  and  the  sounds 

change  from  1-2-3-4 1-2,  etc.,  to   1-2-3 1-2,  etc. 

By  beating  time  to  the  regular  beats  it  is  sometimes  possible  to  note  that 
the  total  rhythm  is  unchanged  by  occasional  ventricular  extrasystoles. 
Such  extrasystoles  correspond  to  impulses  on  the  apex  and  jugular  tracings 
but  not  on  the  carotid. 

The  variations  in  the  force  of  the  extrasystoles  or  in  the  beats  of  the 
absolutely  irregular  pulse  are  great.  Occasionally,  especially  when  the 
extrasystoles  occur  early  in  the  cardiac  cycle  and  there  is  a  high  peripheral 
resistance,  the  intracardiac  pressure  may  not  reach  the  aortic  pressure  and 
the  aortic  valves  are  not  opened.  The  systole  has  been  ineffectual  (Frus- 
trane  contractionen,  Hochaus  and  Quincke).  The  compensatory  pause 
after  these  may  be  so  long  and  the  circulation  may  be  so  poor  that  actual 
syncope  simulating  the  Adams-Stokes  syndrome  (W.  B.  James)  may  take 
place  in  the  interval  between  the  regular  beats.  On  the  other  hand,  a 
great  deal  of  cardiac  energy  has  been  expended  without  opening  the  cardiac 
valves  and  without  propelling  any  blood.    This  increases  the  cardiac  fatigue. 

Bigeminal  and  Trigeminal  Pulses  due  to  Extrasystoles. — Very  common 
forms  of  extrasystolic  irregularity  are  those  in  which  the  extrasystoles 
recur  after  each  regular  beat;  thus  we  may  find  every  beat  followed  by  a 
single  extrasystole  and  compensatory  pause,  so  that  the  pulse  beats  occur 
in  pairs  separated  by  pauses  (pulsus  bigeminus),  or  there  may  be  two 
extrasystoles  following  regularly  after  each  regular  systole  (pulsus  trigem- 
inus), as  in  Fig.  68.  These  may  be  of  either  the  auricular  or  the  ventricular 
type,  dependent  upon  the  site  of  the  origin  of  the  irregularity  or  of  the 
so-called  auriculo(atrio)  ventricular  type  referred  to  below.  As  stated 
above,  it  is  sometimes  difficult  to  differentiate  the  auricular  extrasystolic 


THE  VENOUS  PULSE  AND  ELECTROCARDIOGRAM. 


73 


groups  from  the  youthful  type  of  arrhythmia,  but  this  may  usually  be 
accomplished  by  the  use  of  a  sufficiently  large  dose  of  atropine. 

As  Hering  has  shown,  ventricular  extrasystoles  frequently  disappear 
under  atropine  or  any  other  influence  by  which  the  pulse-rate  is  accelerated, 


Fig.  72. —  Extrasystoles  with  shortened   conduction   time,  supposed   to  arise  in   the  auriculoventricu- 

lar  bundle. 

so  that  the  normal  stimuli  fall  in  at  about  the  periods  at  which  the  abnormal 
stimuli  would  have  fallen.  The  form  of  the  venous  pulse  in  ventricular 
extrasystoles  is,  however,  characteristic. 


Fig.  73. — Variations  in  conduction  time  (a-c)  in  a  case  of  mitral  stenosis. 

Auriculo (A trio)  ventricular  Extrasystoles. — It  is  also  claimed  by  Her- 
ing and  Rihl,  Mackenzie  and  Wenckebach,  Lohmann,  Schmoll,  Mackenzie 
and  Morrow,  and  others  that  extrasystoles  may  arise  in  the  Purkinje  cells 
of  the  conduction  system,  and  that  such  extrasystoles  are 
characterized  by  a  shortening  in  the  conduction  time 
{a-c  interval  on  the  venous  pulse).  Extrasystoles  with  shortened  conduc- 
tion time  are  not  extremely  rare,  and  it  is  possible  that  this  explanation 
may  be  correct,  but  it  is  not  founded  upon  any  direct  experimental  proof. 

Hering,  who  originated  the  doctrine,  observed  such  extrasystoles  occurring  spon- 
taneously in  apes,  but  did  not  clear  it  up  by  any  experiments.  Gaskell  has  shown  in  frojrs 
that  if  the  tissue  at  the  auriculoventricular  junction  was  touched  with  a  probe  a  series  of 
extrasystoles  set  in  in  both  auricles  and  ventricle.  Lohmann  also  observed  them  per- 
sisting after  the  tissue  in  the  vicinity  of  the  His  bundle  had  been  stimulated.  In  a  later 
investigation  upon  the  excised  heart  Lohmann  poisoned  the  region  of  the  venaj  cavte  by 
means  of  cotton  soaked  in  formalin.  He  then  sometimes  saw  extrasystoles  set  in  spon- 
taneously. The  auricles  and  ventricles  sometimes  contracted  simultaneously,  some- 
times there  were  ventricular  extrasystoles. 

Hirschfelder  has  repeatedly  produced  extrasystoles  with  shortened  conduction  time 
by  faradic  stimulation  of  the  auricular  appendix.  The  appearance  of  such  extrasystoles 
after  faradization,  in  excitable  hearts,  in  the  intervals  between  paroxysms  of  tachycardia 
in  man,  etc.,  seems  to  correspond  with  a  state  of  greatly  heightened  excitability.  Whether 
the  actual  stimuli  arise  in  the  cells  of  the  sinus  region  or  in  those  of  the  conduction  system 
is  still  uncertain.  It  is  not  improbable  that  there  may  be  an  increased  irritability  of  all 
the  primitive  cardiac  tissue  (sinus  and  conduction  system),  and  that  in  the  sinus  this  mani- 
fests itself  by  the  generation  of  abnormal  stimuli,  while  in  the  conduction  system  it  is 
shown  by  increased  speed  of  conduction. 

Upon  the  clinical  side  there  is  little  positive  evidence.  Peculiar  extra- 
systoles often  occur  between  attacks  of  paroxysmal  tachycardia,  but  occa- 
sionally also  in  cases  with  simple  valvular  lesions.     Keith  has  found  patches 


74 


DISEASES   OF   THE    HEART   AND    AORTA. 


of  fibrous  myocarditis  in  the  vicinity  of  the  His  bundle  in  cases  which  had 
shown  these  extrasystoles,  and  thinks  that  they  irritated  the  cells  in  the 
vicinity,  but  such  scars  are  very  common,  and  elsewhere  in  the  heart  are 
not  known  to  act  as  irritative  lesions.    Moreover,  the  writer  has  never  been 


I'ffSEC. 


JUG. 


APEX 


BRACK. 


FiQ.  74. — Tracing  showing  absolute  irregular  with  weak  ineffectual  systoles  (/,  /,  /)  which  do  not 
open  the  aortic  valves.  S,  onset  of  ventricular  systole.  Numerals  refer  to  duration  of  cardiac  cycle  in 
tenths  of  a  second.    The  venous  pulse  is  of  the  ventricular  type. 

able  to  produce  them  by  pressure  upon  the  bundle  with  an  Erlanger  clamp, 
injection  of  mercury  into  the  left  branch  of  the  bundle,  etc.  So  that  in 
spite  of  the  interest  in  the  subject  it  must  be  admitted  that  the  occur- 
rence of  extrasystoles  with  shortened  conduction  time  cannot  be  as  yet 
regarded  as  absolute  proof  of  a  lesion  near  the  His  bundle. 


CAR. 


VES. 


AES. 


A- VES. 


A-V  BLOCK 


SINO-AURICULAR  BLOCK 
VAGAL  SLOWING 


Fig.  75. — Diagram  showing  the  alterations  of  rhythm  which  may  cause  a  pulsus  bigeminus. 

indicate  the  incidence  of  stimuli  ori. 


The  arrows 


Various  Types  of  Allorrhythmia  which  may  Result  in  a  Bigeminal  Pulse. 

— It  must  be  borne  in  mind  that  the  bigeminal  pulse  is  not  pathognomonic 
of  any  single  disturbance  of  function,  but  may  occur  in  any  of  the  following 
conditions  (Fig.  75):  (1)  recurring  ventricular  extrasystoles;  (2)  recurring 


THE   VENOUS   PULSE   AND   ELECTROCARDIOGRAM.        75 

auricular  extrasystoles;  (3)  recurring  auriculo ventricular  extrasystoles;  (4) 
recurring  slight  auriculoventricular  heart-block,  the  ventricle  failing  to  follow 
€very  third  beat;  (5)  recurring  sino-auricular  block  ( ?) ,  the  auricles  failing  to 
respond  to  every  third  impulse;  (6)  recurring  vagal  prolongation  of  every 
alternate  diastole.  Similar  conditions  hold  for  the  trigeminal  pulse  except 
that  two  extrasystoles  or  regular  beats  are  interpolated  before  the  pause. 
It  is  evident  that  these  conditions  must  be  carefully  differentiated 
from  one  another  by  means  of  the  venous  tracing  or  electrocardiogram  and 
atropine  tests  before  attempts  to  remedy  them  should  be  begun. 

PARARRHYTHMIAS. 

In  some  of  the  allorrhythmias  separate  rhythms  may  be  noticed  in  the 
different  chambers,  either  conducted  to  one  another  and  interfering  peri- 
odically, or  not  conducted  (heart-block).  Wenckebach,  who  first  called 
attention  to  this,  has  proposed  the  name  pararrhythmia  for  these 
forms.  The  simplest  example  of  this  would  be  the  bigemini.  Another 
example  would  be  seen  if,  without  loss  of  conductivity,  spontaneous  con- 
tractions would  occur  in  the  ventricles  as  the  usual  slow  rate,  and  these 
go  on  simultaneously  with  the  regular  beats  following  the  auricles,  though 
with  occasional  pauses  due  to  interference.  Cushny  has  shown  this  to 
occur  in  digitalis  poisoning,  and  it  is  not  improbable  that  it  may  explain 
many  otherwise  undecipherable  arrhythmias,  though  little  work  has  been 
done  along  these  lines  up  to  the  present. 

ABSOLUTE    ARRHYTHMIA.^ 

Next  to  the  neurogenic  allorrhythmias  the  most  common  form  of  irreg- 
ular heart  action  is  the  permanent  irregularity  (disorderly  rhythm,  Macken- 
zie; pulsus  irregularis  perpetuus,  Hering;  arrhythmia  perpetua,  Gerhardt). 


^^^HH 

t-~ 

-J- — - 

-  I  ^            1 — 



~t- ^ 

+— r- 

CAR. 

1 
c 

c 

c            c 

3.0 

5.0 

z.e> 

4.0 

2.8 

4.0 

3.8 

a 

/\ 

1 

a             /\ 

A       J\ 

JUG. 

c 

c   \— ^'"^ 

BH 

-^^ 

c 

V-^L 

Fig.  76. — Absolute  permanent  irregularity  with  a  wave  preserved  in  a  case  of  mitral  stenosis. 

This  represents,  as  Mackenzie  has  shown,  the  common  type  of  chronic 
arrhythmia  seen  in  old  cases  of  myocarditis  and  of  valvular  lesions.  As  the 
result  of  chronic  stasis  there  is  a  permanently  high  venous  pressure  which 
brings  about  dilatation  and  paralysis  of  the  auricles.  The  a  wave  is  absent 
from  the  venous  tracing  (Mackenzie)  (Fig.  76),  from  the  oesophageal  tracing 
(Hewlett),  and  the  corresponding  wave  has  disappeared  from  the  electro- 
cardiogram (Hering).  There  is  probably  a  perpetual  or  a  transitory  paralysis 
of  the  auricles  (atria).     As  Hering's  electrocardiograms  show,  the  arrhyth- 


'The  term  perpetual  irregularity  is  inaccurate,  since  it  is  sometimes  transitory. 


76  DISEASES   OF   THE    HEART   AND    AORTA. 

mia  is  clue  partly  to  extrasystoles,  which  are  shown  by  their  characteristic 
curves,  and  partly  to  periodic  (respiratory)  alterations  in  the  regular  beats. 
The  site  at  which  the  cardiac  impulse  originates  in  this  irregularity 
is  a  matter  of  some  dispute.  Mackenzie  believes,  without  further  proof, 
that  the  site  of  automaticity  is  shifted  from  the  sinus  region  of  the  auricle 
(atrium)  to  the  cells  of  the  His  bundle  ("nodal  rhythm"),  but  it  has  not 
been  shown  that,  just  because  the  auricular  contraction  and  the  corre- 
sponding negative  wave  are  absent,  the  cardiac  impulse  is  not  arising  in 
the  region  of  the  sinus.  According  to  Mackenzie,  the  auricle  and  ventricle 
are  beating  simultaneously  in  such  cases.  Cushny  (Heart,  vol.  i)  has 
shown  that  such  simultaneous  contractions  actually  occur  in  experimental 
aconite  poisoning.  On  the  other  hand,  v.  Frey  has  shown  that  the 
auricles  become  paralyzed  at  about  20  mm.  Hg  pressure,  and  observations 
by  Dr.  Hooker,  as  well  as  by  Mr.  C.  C.  Cody,  indicate  that  in  cases  with 
permanent  arrhythmia  the  venous  pressure  often  approaches  this  level. 


Fig.  77. — Perpetually  irregular  pulse  with  absence  of  a  wave. 

Radasewsky,  under  Dehio's  direction,  was  the  first  to  call  attention 
to  the  occurrence  of  fibrous  changes  in  the  auricles  under  these  conditions, 
but  the  exact  relations  were  shown  by  Schonberg,  who  studied  careful 
serial  sections  of  the  entire  veno-auricular  region  in  five  cases  that  had 
been  studied  clinically  by  Gerhardt  during  life.  Schonberg  confirms  Rada- 
sewsky and  finds  definite  patches  of  infiltration  about  the  veno-auricular 
border.  On  the  other  hand,  G.  Miiller  has  reported  a  case  in  which  the 
entire  musculature  of  the  auricles  had  disappeared  and  the  rhythm  had 
remained  regular. 

Clinically,  one  sometimes  sees  an  acute  onset  of  absolute  arrhythmia 
with  paralysis  of  the  auricles,  especially  in  the  acute  heart  failure  of  mitral 
stenosis.  This  state  may  last  only  for  a  day  or  so  and  disappear  under 
treatment;  on  the  other  hand,  it  may  last  for  weeks,  perhaps  for  months, 
and  then  disappear.  The  longer  it  persists  the  greater  is  the  probability 
of  serious  changes  and  the  less  that  of  recovery.  On  the  other  hand,  the 
presence  of  an  absolute  and  apparently  permanent  arrhythmia  with  auricu- 
lar paralysis  is  perfectly  compatible  with  a  fair  degree  of  vigor. 

This  is  shown  by  a  medical  student  now  under  the  writer's  care,  who  has  had  an  irreg- 
ular pulse  of  this  type  for  two  years,  during  which  only  occasional  auricular  waves  have 
been  obtainable  upon  his  venous  pulse,  and  these  during  his  periods  of  greatest  vigor.  He 
has  had  slight  shortness  of  breath  on  exertion,  but  no  enlargement  of  the  heart,  murnmrs,  or 
other  signs  of  organic  heart  disease.  His  arrhythmia  did  not  disappear  under  .0007.5  Gm. 
(jV  gr)  atropine  subcutaneously.  The  electrocardiogram  does  not  reveal  any  extrasystoles. 
His  trouble  does  not  date  from  any  acute  infectious  disease  nor  from  any  overstrain  other 
than  the  long  hours  of  work  in  a  hospital.  The  nature  of  the  lesion  and  its  significance 
in  cases  like  this  are  still  mysterious,  but  it  is  possible  that  in  such  cases  there  may  be  a 
patch  of  myocarditis  in  the  sinus  region  of  the  auricle  like  those  shown  by  Schonberg. 


THE  VENOUS  PULSE  AND  ELECTROCARDIOGRAM. 


77 


Permanent  arrhythmia  with  persistence  of  the  auricular  contraction 
(a  wave  upon  the  venous  pulse)  is  met  with  occasionally  in  mitral  disease, 
especially  in   mitral  stenosis;   and  represents  one  form  of  the  so-called 


Fig.  78. — Electrocardiogram  from  a  case  of  perpetual  absolute  arrhythmia,  showing  extrasystole. 
(After  Hering,  Deutsch.  Arch.  f.  klin.  Med.,  xciv.)  E,  extrasystole;  R,  T,  electrical  waves.  The  P 
(auricular)  wave  is  absent. 

"  mitralized  pulse."  In  such  cases  it  may  at  first  seem  absolutely  impos- 
sible to  analyze  the  arryhthmia,  but  from  time  to  time  definite  groups 
of  systoles  may  be  discerned.  Sometimes  these  groups  are  produced  by 
the  occurrence  of  varying  numbers  of  auricular  extrasystoles,  sometimes 
by  the  occurrence  of  a  few  beats  in  which  there  is  doubling  of  the  pulse-rate 
and  shortening  of  the  conduction  time,  just  as  is  seen  in  paroxysmal 
tachycardia.  Since  Hering  has  demonstrated  the  extrasystolic  origin 
of  the  absolute  arrhythmia  with  auricular  paralysis  (Mackenzie's  ''nodal 
rhythm"),  and  since  Hirschfelder  has  produced  the  latter  in  experimental 
mitral  stenosis  by  bringing  about  extreme  stasis  in  the  left  auricle,  it 
seems  not  impossible  that  the  question  of  auricular  paralysis  may  be  one 
of  the  degree  rather  than  of  the  character  of  the  disturbance. 

The  prognostic  importance  of  a  permanent  arrhythmia  with  auricular 
paralysis  depends,  like  all  other  cardiac  conditions,  chiefly  upon  its  effect 
upon  cardiac  function. 


MECHANICAL    EFFECT    OF    ARRHYTHMIA    IX    THE    CIRCULATION. 

The  mechanical  effect  of  any  arrhythmia  is  to  s  1  o  w  the  circu- 
lation, as  may  be  easily  seen  from  the  volume  curve  of  the  heart  during 
a  period  of  irregularity. 
This  slowing  in  itself  tends 
to  bring  on  cyanosis,  in- 
crease the  CO2  in  the  blood, 
and,  as  Cameron  has  shown, 
to  diminish  the  tone  of  the 
heart  muscle  in  this  way. 
On  the  other  hand,  the  long- 
pauses  cause  an  increase  of 
pressure  in  the  veins,  and 
the  influx  of  venous  blood  under  a  relatively  increased  pressure  acting 
upon  cardiac  muscle,  whose  tone  is  diminished,  tends  to  overdistend  the 
heart  (as  seen  in  Fig.  79) .     The  overdistention,  by  increasing  the  diameter 


Fig.  79. — Effect  of  arrhythmia  on  the  circulation,  blood- 
pressure,  and  volume  of  the  ventricles.  Tracing  from  a  dog's 
heart  stimulated  irregularly  with  induction  shocks.  /,  /,  /. 
ineffectual  systoles;  DIL,  dilatation.  Upstrokes  on  volume 
curve  represent  outflow  from   the  ventricles. 


78  DISEASES   OF   THE    HEART    AND    AORTA. 

of  the  ventricular  chamber,  increases  the  hydrostatic  pressure  upon  its 
walls  and  causes  it  to  work  at  a  disadvantage.  Thus  is  established  the 
vicious  circle  of  the  irregular  heart: 

Overfilling  of  heart 

T  1 

Slowing  of  circulation -^Irregularity 

The  effect  is  most  marked  in  the  auricles,  where  tone  changes  show  themselves  in  more 
marked  degree  than  in  the  ventricles,  and  the  diminution  in  their  tonicity  hastens  their 
paralysis.  When  the  auricles  are  paralyzed,  the  genesis  of  efficient  stimuli  becomes  more 
difficult,  it  is  harder  to  accelerate  the  pulse  during  excerise,  etc.,  and  consequently  it 
becomes  easier  for  COj  to  accumulate  in  the  blood  in  the  irregular  than  in  the  regular  heart, 
and  the  heart  in  this  condition  is  per  se  permanently  weakened. 

Effect  of  Digitalis  in  Absolute  Arrhythmia. — The  good  effect  of  digi- 
talis in  this  condition  lies  not  in  affecting  the  rhythmicity  but  particularly 
in  restoring  tone  and  force  of  the  heart-beat,  thus  re- 
versing the  vicious  circle.  The  pulse  becomes  more  regular,  sometimes 
entirely  regular.  When  the  rhythmicity  is  destroyed  by  permanent  paraly- 
sis of  the  auricles  it  never  returns,  but  the  general  cardiac  condition  may 
be  benefited  by  increase  in  tone  and  strength.  On  the  other  hand,  when 
the  muscle-fibres  are  in  too  bad  condition,  they  are  oversensitive  to  digitalis 
and  a  small  dose  causes  them  to  pass  not  into  the  first  but  into  the  second 
or  third  stage  of  digitalis  poisoning, 

PAROXYSMAL   TACHYCARDIA. 

Another  group  of  allorrhythmias  which  may  be  classed  with  the  extra- 
systoles  is  that  in  which  there  is  more  or  less  paroxysmal  increase  in  pulse- 
rate,  frequently  amounting  to  exact  doubling  of  the  rate, 
suddenly   taking   place    and   suddenly   subsiding. 

This  condition  is  seen  in  paroxysmal  tachycardia  (Hoffmann)  and  in  paroxysmal 
irregularity  (Cushny  and  Edmunds),  and  in  the  latter  condition  has  been  shown  to  be 
associated  with  fibrillation  of  the  auricles.  Exf)erimentally  it  can  be  brought  on  by  stimu- 
lating the  auricles  with  a  strong  faradic  current,  the  auricles  then  going  into  very  rapid 
more  or  less  fibrillary  contractions,  the  ventricles  following  at  a  fairly  regular 
rate  which  is  almost  exactly  double  the  previous  rate,  this  rhythm  persisting  for  several 
minutes  after  the  faradization  has  been  stopped  and  then  suddenly  halving.  During  its 
continuance  it  may  or  may  not  be  stopped  by  maximal  stimulation  of  the  vagus,  just  as 
is  the  case  clinically  in  paroxysmal  tachycardia,  but  seems  to  yield  at  once  to  strophan- 
thus  intravenously.  The  nature  of  this  sudden  doubling  is  peculiar.  It  also  occurs  in 
the  ventricle  upon  faradizing  the  ventricular  muscle  directly,  and  similar  exact  doubling 
and  exact  halving  of  rate  have  been  observed  in  the  frog  by  Engelmann  and  in  the 
mammal  by  Trendelenberg.      (See  Part  IV,  Chapter  I.) 

BIBLIOGRAPHY. 

For  general  discussions  of  alterations  of  cardiac  rhythm  the  reader  may  consult: 
Wenckebach,  K.  F.:  Die  Arhythmie  als  Ausdruck  bestimmter  Functionsstorungen  des 

Herzens,  Leipz.,  1903.     Les  irregularity  du  cceur.  Arch,  des  malad.  du  coeur..  Par., 

1908,  i,  65. 
Mackenzie,  J.:  The  Study  of  the  Pulse  and  Movements  of  the  Heart,  Lond.,  190.3.     New 

Methods  of  Studying  Affections  of  the  Heart,  Brit.  M.  J.,  Lond.,  1905,  i,  519,  587, 

702,  759,  812.    Diseases  of  the  Heart,  Lond.,  1908. 


THE   VENOUS    PULSE    AND   ELECTROCARDIOGRAM.        79 

Hirschfelder,  A.  D.:  Graphic  Methods  in  the  Study  of  Cardiac  Diseases,  Am.  Jour.  M. 
Sc,  Phila.,  1906,  cxxxii,  378.  Recent  Studies  upon  the  Circulation  and  their  Im- 
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Hewlett,  A.  W.:  Some  Common  Cardiac  Arrhythmias,  Internat.  Clin.,  Phi.a.,  1907,  17th 
ser.,  iv,  47. 

Gerhardt,  D.:  Die  Unregelmassigkeiten  des  Herzschlages,  Ergebn  d.  innere  Med.,  Berl., 
1908,  ii,  418. 

Dock,  Geo.:  Recent  Advances  in  the  Study  of  Heart  Disease,  Wisconsin  M.  J.,  Aug.,  1907. 

Bard,  L.:  Des  divers  types  d'arhythmie  cardiaque  observes  en  clinique,  Sem.  m^d..  Par., 
1909. 

Hoffmann,  A.:  Ueber  die  klinische  Bedeutung  der  Herzarhythmie, -Deutsch.  med.  Wchn- 
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krankheiten,  Deutsch.  med.  Wchnschr.,  Leipz.,  1908,  xxxiv,  13. 

Hunt,  R.:  Direct  and  Reflex  Acceleration  of  the  Mammalian  Heart,  Am.  J.  Physiol., 
Bost.,  1899,  ii,  395. 

Hooker,  D.  R.:  May  Reflex  Cardiac  Acceleration  Occur  Independently  of  the  Cardio- 
inhibitcry  Centre  ?  ibid.,  1907,  xix,  417. 

Mackenzie,  J.:  The  Study  of  the  Pulse  and  Movements  of  the  Heart,  Lond.,  1903. 

Frangois-Franck,  Ch.  A.:  Contribution  a  I'etude  experimentale  des  nevroses  reflexes 
d'origine  nasale,  Arch,  de  physiol.  de  I'homme,  Par.,  1889,  5  ser.,  i,  538.  Contri- 
bution a  I'etude  de  I'innervation  vasodilatatrice  de  la  muqueuse,  ibid.,  1889,  i. 

Koblanck  and  Roeder,  H.:  Experimentelle  Untersuchungen  zur  reflektorischen  Herz- 
arhythmie, Arch.  f.  d.  ges.  Physiol.,  Bonn,  1908,  cxxv,  377. 

Stadler,  E.,  and  Hirsch,  C:  Meteorismus  und  Kreislauf,  Mitth.  a.  d.  Grenzgeb.  d.  Med. 
u.  Chir.,  Jena,  1906,  xv,  449. 

Reyfisch:  Klinische  und  experimentelle  Erfahrungen  ueber  Reizungen  des  Herzvagus, 
Berl.  Win.  Wchnschr.,  1905,  1468. 

Reissner,  O.:  Ueber  unregelmassige  Herztatigkeit  auf  psychischer  Grundlage,  Ztschr.  f. 
khn.  Med.,  Berl.,  1904,  liii,  234. 

Einthoven,  W.,  Flohil,  A.,  and  Battaerd,  P.  J.  T.  A.:  On  Vagus  Currents  Examined  with 
the  String  Galvanometer,  Quart.  Jour.  Exper.  Physiol.,  Lond.,  1908,  i,  243. 

Eyster,  J.  A.  E.:  Clinical  and  Experimental  Observations  upon  Cheyne-Stokes  Respira- 
tion, Jour.  Exper.  M.,  New  York  and  Lancaster,  1906,  viii,  565. 

Kussmaul,  A.:  Ueber  schwielige  Mediastino-pericarditis  und  paradoxen  Puis,  Berl.  klin. 
Wchnschr.,  1873,  x,  433,  445,  461. 

Riegel,  F.:  Ueber  extrapericardiale  Verwachsungen,  ibid.,  1877,  xiv,  657. 

Keith,  A.,  and  Flack,  and  Schonberg:  See  Chapter  I. 

Hewlett,  A.  W.:  Digitalis  Heart-block,  J.  Am.  M.  Assoc,  Chicago,  1907,  xlviii,  47. 

Erlanger,  J.,  and  Blackman,  J.  R.:  A  Study  of  the  Relative  Rhythmicity  and  Conduc- 
tivity in  Various  Regions  of  the  Auricles  of  the  Mammalian  Heart,  Am.  J.  Physiol., 
Bost.,  1907,  xix,  125. 

Hoffmann,  Aug.:  See  chapter  on  Paroxysmal  Tachycardia. 

Hirschfelder,  A.  D.,  and  Eyster,  J.  A.  E.:  Extrasystoles  in  the  Mammalian  Heart,  Am.  J. 
Physiol.,  Bost.,  1907,  xviii,  222. 

Kraus,  Fr.,  and  Nikolai:  Ueber  das  Elektrokardiogramm  unter  normalen  und  patho- 
logischen  Verhaltnissen,  Berl.  klin.  Wochnschr.,  1907,  765,  811. 

Kahn,  R.  H.:  Ueber  das  Elektrokardiogramm  kiinstlich  ausgeloster  Herzschlage  Zentralbl. 
f.  Physiol.,  Leipz.  and  Vienna,  1909,  xxiii,  444. 

Hewlett,  A.  W.:  Heart-block  in  the  Ventricular  Walls,  Arch.  Int.  Med.,  Chicago,  1908, 
ii,  139. 

Barker,  L.  F.,  Hirschfelder,  A.  D.,  and  Bond,  G.  M.:  Effects  of  Cutting  the  Branch  of  the 
Left  His  Bundle  going  to  the  Left  Ventricle,  Trans.  Assoc.  Am.  Phys.,  Phila.,  1909.  Also- 
Barker,  L.  F.,  and  Hirschfelder,  A.  D.:  Arch.  Int.  Med.,  Chicago,  1909,  iv,  193. 

Aschoff,  L.,  and  Tawara,  S.:     See  chapter  on  Acute  Myocarditis. 

Hirschfelder,  A.  D.:  Observations  upon  Paroxysmal  Tachycardia,  Johns  Hopkins  Hosp. 
Bull.,  Bait.,  1906,  xvii,  337. 

Hering,  H.  E.:  Ueber  Herzalternans,  Muenchen.  med.  Wochnschr.,  1908,  Iv,  1417. 

Mackenzie,  J.:  See  chapter  on  Angina  Pectoris. 

Wenckebach,  K.  F. :  Beitriige  zur  Kenntniss  der  menschlichen  Herztatigkeit,  Arch,  f^ 
Physiol.,  1906;  1907,  i. 


80  DISEASES   OF   THE   HEART    AND    AORTA. 

Engelmann:    Ueber  die  Leitung  der  Bewegungsreize  im  Herzeii,  Arch.  f.  d.  ges.  Physiol., 

Bonn,  1894,  ivi,  149.    Ueber  die  Ursprung  der  Herzbewegungen,  ibid.,  Ixv. 
Cushny,  A.  R.,  and  Matthews,  S.  A.:  On  the  Effects  of  Electrical  Stimulation  of  the  Mam- 
malian Heart,  Jour.  Physiol.,  Camb.,  1897,  xxi,  214. 
Hirschfelder,  A.  D.:  Inspection  of  the  Jugular  Vein;    its  Value  and  its  Limitations  in 

Functional  Diagnosis,  Jour.  Am.  M.  Assoc,  Chicago,  1907,  xlviii,  1105. 
Lewis,  T.:  Single  and  Successive  Extrasystoles,  Lancet,  Ix)nd.,  1909,  i. 
Muller,  Fr.:  Nervous  Affections  of  the  Heart,  Arch.  Int.  Med.,  Chicago,  1908,  i,  1. 
Mackenzie,  J.:  Diseases  of  the  Heart,  Lond.,  1908. 
Knoll,  Ph.:  Ueber  die  Veraenderungen  des  Herzschlages  bei  reflectorischer  Erregung  des 

vasomotorischen   Nervensystems,    sowie   bei   Steigerung   des   intracardialen   Drucks 

iiberhaupt,  Sitzungsber.  d.  k.  Akad.  d.  \\'issensch.,  Wien,  Abth.  Ill,  1872,  Ixv-lxvi,  195. 
Marey:  La  circulation  du  sang  a  I'etat  physiologique  et  dans  les  maladies,  Par.,  1881. 
Hering,  H.  E.:  Zur  experimentellen  Analyse  des  unregelmassigen  Herzschlages,  Arch.  f. 

d.  ges.  Physiol.,  Bonn,  1900,  Ixxxii.     Ueber  continuierliche  Herzbigeminie,  Deutsch. 

Arch.  f.  klin.  Med.,  Leipz.,  1904,  Ixxix,  175.     Ergebnisse  experimenteller  und  klin- 

ischer   Untersuchungen   ueber  den   Vorhofvenenpuls   bei    Extrasystolen,   Ztschr.   f. 

exper.  Path.  u.  Therap.,  Berl.,  1905,  i,  26;  also  his  pupils. 
Rihl,  J.:  Experimentelle  Analyse  des  Venenpulses  bei  den  durch  Extrasystolen  verur- 

sachten  Unregelmassigkeiten  des  Saugethier  herzens,  ibid.,  1905,  i,  43. 
Pan,  O.:  Ueber  das  Verhalten  des  Venenpulses  bei  den  durch  Extrasystolen  verursachten 

Unregelmassigkeiten  des  menschlichen  Herzens,  ibid.,  1905,  i,  56. 
Hirschfelder,  A.  D.:  The  Volume  Curve  of  the  A'entricles  in  Experimental  Mitral  Stenosis 

and  its  Relation  to  Physical  Signs,  Johns  Hopkins  Hosp.  Bull.,  Bait.,  1908,  xix,  319. 
Mackenzie,  J.:  The  Extrasystole,  Quart.  J.  M.,  Oxford,  1908,  i,  481. 
Gerhardt,  D.:  Beitrag  zur  Lehre  von  den  Extrasystolen,  Deutsch.  Arch.  f.  klin.  Med., 

Leipz.,  1905,  Ixxxii,  509. 
Hoffmann,  Aug.:  Arhythmie  des  Herzens,  Deutsch.  med.  Wchnschr.,  Leipz.,  1906,  xxxii, 

1682.      Ueber    die    Entsthung    der    Extrasystolen    irregularitat,    Muenchen.   med. 

Wchnschr.,  1907,  liii,  1987. 
Dehio,  K.:  Einfluss  des  Atropins  auf  arhythmische  Herztatigkeit,  Deutsch.  Arch.  f.  kUn. 

Med.,  Leipz.,  1894,  lii,  97. 
Hering,  H.  E. :  Experimentelle  L^ntersuchungen  ueber  Herzunregelmassigkeiten  an  Affen, 

Ztschr.  f.  exper.  Path.  u.  Therap.,  Berl.,  1906,  ii,  525. 
Hering,  H.  E.,  and  Rihl,  J.:  Ueber  atrioventrikulare  Extrasystolen,  ibid.,  1906,  ii,  510. 
Gaskell,  W.  H.:  The  Properties  of  Cardiac  Muscle,  Schafer's  Text-book  of  Physiology, 

Lond.,  1900,  ii. 
Lohmann,  A.:  Zur  Automatie  der  Briickenfasem  des  Herzens,  Arch.  f.  Physiol.,  Leipz., 

1904,  431 ;    and  Supplbd.,  265.     Ueber  der  Funktion  der   Briickenfasem   an   Stelle 

der  grossen  Venen  die  Fiihrung  der  Herztatigkeit  beim  Saugetiere  zu  ubemehmen. 

Arch.  f.  d.  ges.  Physiol.,  Bonn,  1908,  cxxiii,  628. 
Mackenzie,  J.:  Inception  of  the  Rhythm  of  the  Heart  by  the  Ventricles,  Brit.  M.  J.,  Lend., 

1904,  i,  529.     Abnormal  Inception  of  the  Cardiac  Rhythm,  Quart.  J.  M.,  Oxford, 

1907,  i,  39. 
Mackenzie,  J.,  and  Wenckebach,  K.  F.:  L'eber  an  der  Atrioventrikulargrenze  ausgeloste 

Systolen  beim  Menschen,  Arch.  f.  Phj'siol.,  Leipz.,  1905. 
Schmoll,  E. :  Paroxysmal  Tachycardia,  Am.  J.  M.  Sc,  Phila.  and  N.  York,  1907,  cxxxiv, 

662. 
Mackenzie,  R.,  and  Morrow,  W.  S.:  Cardiac  Arrhythmia  due  to  Extrasystoles  Originating 

in  the  Bundle  of  His,  Am.  J.  M.  Sc,  Phila.  and  N.  York,  1908,  cxxxv,  534. 
Cushny,  A.  R.:  See  chapter  on  the  Action  of  Drugs. 

Hering,  H.  E.:  Ueber  die  haufige  Kombination  von  Kammervenenpuls  mit  Pulsus  irreg- 
ularis perpetuus,  Deutsch.  med.  Wchnschr.,  Leipz.,  1906,  213. 
Gerhardt,  D.:  Arhj-thmis  perpetua  des  Puis,  Deutsch.  med.  Wchnschr.,   Leipz.,   1907, 

xxxiii,  448. 
Hewlett,  A.  W.:  On  the  Interpretation  of  the  Positive  Venous  Pulse,  J.  M.  Research, 
1907-8,  xvii,  119.     Clinical  Observations  on  Absolutely  Irregular  Hearts,  J.  Am.  M. 

Ass.,  Chicago,  1908,  Ii,  655. 
Theopold,  J.:  Ein  Beitrag  zur  Lehre  von  der  Arhj-thmia  perpetua,  Deutsch.  Arch.  f.  klin. 

Med.,  Leipz.,  1907,  xc,  77. 


THE   VENOUS   PULSE    AND   ELECTROCARDIOGRAM.        81 

Hering,   H.  E.:  Das  Elektrocardiogramm  des  Pulsus  irregularis  perpetuus,  ibid.,   1908, 

xciv,  205. 
Radasewsky:  See  chapter  on  Chronic  Myocarditis.     Ueber  die  Muskelkrankungen  der 

Vorhofe  des  Herzens,  Ztschr.  f.  klin.  Med.,  Berl.,  xxvii. 
Schonberg,  S.:   U^eber  Veraenderungen  im  Sinusgebiete  des  Herzens  bei  chronischer  Ar- 

rhythmie,  Frankf.  Ztschr.  f.  Path.,  1908,  ii,  153. 
Miiller,  G.:    Ungewohnliche   Dilatation  des   Herzens   und   Ausfall   der  Vorhofsfunktion, 

Ztschr.  f.  klin.  Med.  Berl.,  Ivi,  520. 
Quincke,  and  Hochhaus,  J.:  Ueber  frustrane  Herzcontractionen,  Deutsch.  Arch.  f.  klin. 

Med.,  Leipz.,  1894,  liii,  414. 
James,  W.:  Clinical  Study  of  Some  Arrhythmias  of  the  Heart,  Am.  Jour.  M.  Sc,  Phila. 

and  N.  York,  1908,  cxxxvi,  469. 
Hirschfelder,  A.  D.:  Contributions  to  the  Study  of  Auricular  Fibrillation,   Paroxysmal 

Tachycardia,    and    the    so-called    Auriculo(Atrio)ventricular    Extrasystoles,    Johns 

Hopkins  Hosp.  Bull.,  Bait.,  1908,  xix,  322. 
Hoffmann,  A.:  Neue  Beobachtungen  ueber  Herzjagen,  Deutsch.  Arch.  f.  klin.  Med.,  1903, 

Ixxviii,  39. 
Cushny,  A.  R.,  and  Edmunds,  C.  W.:  Paroxysmal  Irregularity  of  the  Heart  and  Auricular 

Fibrillation,  Am.  Jour.  M.  Sc,  Phila.,  1907,  cxxxiii,  66;    and  Studies  in  Pathology, 

Quatercentenary  Public,  Aberdeen  Univ. 
Engelmann,  1.  c. 
Trendelenberg,  W.:  Untersuchungen  ueber  das  Verhalten  des  Herzmuskels  bei  rhythm- 

ischer  elektrischer  Reizung,  Arch.  f.  Physiol.,  Leipz.,  1903,  271. 


V. 
X-RAY  EXAMINATION. 

The  discovery  of  the  X-rays  by  Rontgen  in  1895  introduced  a  new 
era  in  cardiac  diagnosis.  By  this  means  we  can  now  actually  see  the  heart, 
observe  its  outlines  with  accuracy,  and  note  the  changes  of  position  and 
of  contour  with  different  phases  of  respiration,  and  even  to  a  certain  extent 
the  changes  from  systole  to  diastole.  All  these  data,  when  obtained  with 
proper  precautions,  are  absolutely  accurate,  and  have  greatly  supplemented 
the  observations  made  b}^  percussion.' 

METHODS    OF    EXAMINATION. 

Most  of  the  facts  desired  in  the  study  of  the  circulatory  system  with 
the  X-ray  may  be  gained  by  means  of  inspection  with  the  fluoroscope, 
a  screen  of  barium  platinocyanide  or  calcium  tungstate  which  is  rendered 
luminous  wherever  the  X-rays  strike  it. 

A  tube  of  low  vacuum  (''soft  tube")  should  be  used,  one 
which  shows  the  bones  of  the  hand  black  without  re- 
vealing their  internal  structure,  and  the  tissues  of  the  hand  a 
fairly  dark  gray.  The  patient's  chest  wall  should  be  at  least  50  cm.  from 
the  screen.  Recently  the  usual  distance  has  been  increased  to  2  M.  (6^ 
ft.),  at  which  the  rays  are  almost  parallel. 

It  is  sometimes  best  to  interpose  a  lead  screen,  with  adjustable  opening,  between  the 
patient  and  the  tube  in  order  to  cut  off  all  the  rays  except  those  emanating  from  a  small 
part  of  the  anticathode,  thereby  securing  the  greatest  possible  definition  of  focus.  Indeed, 
Immelmann  found  greatest  definition  when  the  opening  in  the  lead  screen  was  only  1  cm. 
Often  a  lead  cyhnder  (Albers-Schoenberg)  is  very  satisfactory.  It  is  also  important  that 
no  large  objects  be  placed  near  the  cathode,  as  rays  striking  these  may  also  generate 
secondary  rays  which  affect  the  fluoroscope  or  photographic  plate  and  thus  blur  the  outline 
of  the  original  image  (Walter).  P^or  securing  sharp  images  it  is  preferable  to  keep  a 
number  of  tubes  with  vacua  of  different  degrees  wliich  may  be  interchanged,  rather  than 
change  the  vacuum  in  each  tube.  Changing  the  latter  shortens  the  life  of  the  tube  by 
heating  the  platinum  target  and  causing  the  latter  ultimately  to  become  bent,  so  that  the 
rays  are  not  reflected  uniformly  from  its  surface. 

The  X-ray  image  is  a  true  shadow  formed  by  the  cutting  off  of  rays 
and  not  by  their  refraction,  and  the  shadow  is  magnified  in  proportion  as 
the  object  is  nearer  to  the  tube  or  farther  from  the  fluoroscopic  screen. 

*  Examinations  with  the  X-ray  require  a  very  special  technic,  for  which  the  student 
is  advised  to  consult  the  special  text-books  upon  the  subject,  especially: 

Albers-Schoenberg:  Die  Rontgentechnik,  Hamburg,  1906. 

Gocht,  H.:  Handbuch  der  Rontgenlehre  zum  Gebrauche  fiir  Mediziner,  2te  Aufl.. 
Stuttgart,   1903. 

Williams,  F.  H.:  The  Rontgen  Rays  in  Medicine  and  Surgery,  New  York,  1903. 

Beck,  C:  Rontgen-ray  Diagnosis  and  Therapy. 

Kassabian:  Rontgen  Rays  and  Electro-Therapeutics,  Phila.,  1909. 
82 


X-RAY   EXAMINATION.  83 

In  fluoroscopic  examination  it  is  most  important  for  the  observer  to  accustom  his 
eyes  to  the  darkness  before  turning  on  the  current.  It  is  a  well-proved  physiological  fact 
that  the  longer  the  sojourn  in  darkness  the  greater  the  delicacy  of  vision.  Hence  the  exami- 
ner's Aasion  is  improved  by  closing  or  bUndfolding  his  eyes  or  by  going  into  a  dark  room 
some  ten  or  fifteen  minutes  before  the  patient;  and  the  examining  room  should  be  lighted 
only  enough  to  permit  the  patient  to  undress  and  assume  the  proper  position.  The  exami- 
ner may  also  keep  his  head  under  a  dark  hood  or  wear  heavily  smoked  glasses  during  this 
time  so  as  to  accustom  his  eyes  to  the  darkness. 

In  looking  over  the  areas  of  light  and  shadows  each  region  should  be 
studied  carefully  and  in  detail,  the  size  and  shape  of  the  shadow,  the  clear- 
ness of  the  outline,  and  the  distribution  of  areas  of  half  shadows  as  well  as 
of  full  shadows.  Not  of  least  importance  are  the  so-called  pulmonary 
figures,  the  half-tone  shadows  of  pulmonary  vessels,  of  bronchial  glands, 
and  of  strands  of  adhesions.'  Not  only  the  full  shadows  but  especially 
these  half  shadows  should  be  examined  with  care,  for  an  interpretation 
not  apparent  at  first  may  become  clear  after  a  few  minutes'  observation. 

Radiographers  are,  moreover,  in  the  habit  of  looking  at  the  fluoroscope  through  half- 
closed  eyes  in  order  to  intensify  the  contrast.  This  may  be  further  intensified  by  the  use 
of  dark  glasses.  The  writer  has  also  found  it  very  useful  to  look  at  the  shadow  or  skiagraph 
through  a  biconcave  lens  which  at  once  sharpens  the  contours  and  intensifies  the  contrasts. 

Often  an  area  may  be  indefinite  during  quiet  breath- 
ing or  expiration  and  become  quite  tlefinite  on  forced 
deep  inspiration,  or  it  may  become  so  by  simply  turning 
the  patient  so  that  the  rays  pass  through  his  bodyin 
a  different  direction.  These  and  similar  precautions,  like  a  care- 
ful physical  examination,  reveal  the 
unsuspected,  and  distinguish  the 
skilled  examiner  from  the  unskilled. 

The  Cardiac  Shadow. — The  heart 
shadow  thrown  upon  a  screen  at  the 
front  of  the  chest  is  shown  in  Fig.  81. 
It  will  be  noted  that  the  outline  of 
the  shadow  closely  resembles  the 
area  of  relative  dulness  on  percus- 
sion, except  that  the  former  extends 
upward  over  the  manubrium  sterni, 
where  it  is  due  to  the  presence  of 

the     latter    and    of     the    great    vessels  Fig.  so.— Radiograph  of  normal  chest.     (After 

,         ,      .  . ,       ,  J        X      ii  1         V.  Ziemmsen  and  Rieder.;    Tube  behind  the  chest 

and  not  of  the  heart.    In  the  second      piate  in  front. 

left    interspace    the    shadow 

of    the    pulmonary    artery    is    seen^    and   in    the   second    right 

that    of    the    aorta.     Occasionally  a  small  prominence  is  seen  to  the  left 

of  the  sternum  arising  at  the  arch  of  the  aorta.     This  is  sometimes  mistaken 

for  an  aneurism,  but  if  the  patient  be  turned  a  little  it  will  be  seen  to  be 

due  to  the.  curving  of    the  aorta  (Holzknccht). 

Oblique  Illuminations. — Much  can  be  learned  by  turning  the  patient 
about  and  examining  him  in  several  planes,  as  was  first  performed 
by  V.  Criegern  and  Holzknecht  (1.  c),  and  later  by  Rieder,  who  suggested  the 


See  chapter  on  Adherent  Pericardium. 


84 


DISEASES    OF   THE    HEART    AND    AORTA. 


following  cardinal  directions  (Fig.  81):  (1)  dorso ventral ;  (2)  ventrodorsal; 
(3)  sagittal  from  right;  (4)  sagittal  from  left;  (5)  from  right  posterior  to 
left  anterior;  (6)  from  left  posterior  to  right  anterior;  (7)  from  left  anterior 
to  right  posterior;   (8)  from  right  anterior  to  left  posterior. 


Fig.  81. — X-ray  shadows  in  different  axes  of  the  body.  (Modified  from  Holzkrecht.)  The 
arrows  show  the  direction  of  illumination  and  position  of  the  tube  corresponding  to  the  shadow. 
AO,  aorta;  PA,  pulmonary  artery;  LA,  left  auricle;  RA,  right  auricle;  LV,  left  ventricle;  RV,  right 
ventricle.    In  3  there  is  a  metal  sound  in  the  cesophagus. 


By  the  examination  in  these  planes  every  part  of  the  heart  can  be 
brought  into  view,  even  the  left  auricle,  which  escapes  observation  in  almost 
all  other  methods  of  examination  but  appears  quite  clearly  when  the  tube 
is  placed  at  the  back  or  behind  the  right  scapula.  The  oblique  and  trans- 
verse examinations  should  never  be  omitted. 


X-RAY  EXAMINATION. 


85 


THE    ORTHODIAGRAPH. 

The   shadow  of  the  heart  and  vessels  upon  the  screen  or  plate  is 
always    larger  than   the   objects  themselves.     In   order  to   obviate  this 

when  measuring  out  the  heart  F. 
Moritz  devised  an  instrument  known 
as  the  orthodiagraph  (Fig.  82). 


Fig.  82.- 


-A  simple  form  of  orthodiagraph. 

(After  Gillet.) 


Fig.  83. — Diagram  showing  the  use  of  the  ortho- 
diagraph. 1,  first  position;  2,  second  position;  P, 
pencil;   FLUOR,  fluorescent  screen. 


In  the  orthodiagraph  the  fluorescfent  screen  and  X-ray  tube  are  fixed  upon  each  arm 
of  a  large  fZ-shaped  frame  in  such  a  way  that  the  patient  may  stand  or  lie  between  the 
two  arms  of  the  U  and  the  rays  thus 
pass  through  his  body  to  the  screen. 
At  the  point  upon  the  screen  which  is 
exactly  opposite  to  the  centre  of  the 
anticathode  or  target  of  the  tube,  a 
small  hole  is  pierced,  and  a  skin  pencil 
is  fixed  in  place  here  so  that  the  site  of 
this  spot  can  be  marked  upon  the  body 
of  the  patient.  The  whole  [/-shaped 
frame  bearing  the  tube  and  fluoroscope 
is  movable  in  two  directions  by  any 
one  of  a  variety  of  mechanisms,  so  that 
the  perpendicular  ray  can  be  brought 
opposite  any  desired  point.  A  series  of 
points  corresponding  to  the  exact  con- 
tour can  thus  be  marked  off,  and  when 
these  are  joined  with  lines  the  exact 
outline  of  the  heart  is  repre- 
sented. As  shown  by  Fig.  83,  this 
furnishes  a  means  of  determining  the 
size  of  the  heart  or  any  organ  with 
absolute  accuracy. 

The  outlines  and  mobility  of  the  heart  thus  obtained  are  discussed 
on  page  97. 

It  is  also  possible  with  the  fluoroscope  to  watch  the  individual  con- 
tractions of  the  heart  and  to  note  the  changes  in  size  due  to  systole  and 


Fig.  84. — Orthodiagraphic  outline  of  normal  heart, 
showing  Moritz's  conjugates.  MR,  midline  to  right 
border  (greatest  distance);  ML,  midline  to  left  border; 
L,  oblique  longitudinal;  Q,  transverse;  numerals  indi- 
cate centimetres. 


86  DISEASES    OF   THE    HEART    AND    AORTA. 

diastole,  but  this  is  very  difficult  and  can  rarely  be  done  with  satisfactory 
accuracy.  On  the  other  hand,  the  contractions  of  the  auricles  can  be  seen 
with  considerable  definiteness,  and  dissociation  of  rhythm,  heart- 
block,  can  often  be  diagnosed  in  this  way  by  sim- 
ple  inspection    (Kraus,   Gibson) . 

PERMANENT    RADIOGRAPHS. 

For  obtaining  permanent  photographs  a  "  medium  soft "  tube  (Moritz 
scale  W  6  B  W  5)  is  used  in  connection  with  a  Wehnelt  electrolytic  inter- 
rupter and  an  induction  coil  with  proper  self-induction  yielding  a  40  to  60 
cm.  spark.  The  patient  is  laid  upon  a  table  with  the  tube  above  or  below 
him,  as  is  most  suitable  to  the  purpose  of  the  examination.  In  order  to 
absolutely  immobilize  him  it  is  well  to  support  the  shoulders  upon  sand 
bags.  He  may  also  be  examined  standing  by  immobilizing  the  shoulders 
to  prevent  blurring  of  the  picture.  Magnification  of  the  shadow  may  be 
obviated  by  placing  the  tube  at  a  distance  of  2  M.  Skiagraphs  of  the  chest 
made  with  very  short  exposures  have  proved  particularly  valuable,  since 
they  give  greater  definition  (Rieder). 

BIBLIOGRAPHY. 

Rontgen,  W.  K.:  A  New  Form  of  Radiation,  Science,  N.  York  and  Lancaster,  1896,  N.  S. 

iii,  726  and  729. 
Barker,  Geo.  F.:  The  Rontgen  Rays.    Memoirs  by  Rontgen,  Stokes,  and  Thompson,  N.  Y. 

and  Lond.,  1899. 
Michelson,  A.  A.:  Theory  of  the  X-rays,  Am.  Jour.  Sc,  1896,  4th  ser.,  i,  312. 
Rowland,  H.:  Notes  of  Observations  on  the  Rontgen  Rays,  ibid.,  1896,  4th  ser.,  i,  247. 
For  details  regarding  the  secondary  rays  see: 
Walter,  B.:  Physikalisch  technische  Mitteilungen,  Fortschr.  a.  d.  Geb.  d.  Rontgenstrah- 

len,  Hamb.,  1900,  i,  82. 
Faulhaber :    Ueber  eine  durch  Sekundarstrahlung  bedingte  Erscheinung  auf  Rontgen- 

platten,  ibid.,  1903,  v-i,  93. 
Holzknecht,  G.:  Die  rontgologische  Diagnostik  der  Erkrankungen  der  Brusteingeweide, 

Hamb.,   1901.     Das  radiologische  Verhalten  der  normalen  Brustaorta,   Wien.  klin. 

Wchnschr.,  1900. 
Cotton,  W.:  Some  Principles  and  Fallacies  of  X-ray  Interpretation,  Practitioner,  Lond., 

1906,  Extra  No.  on  X-rays,  100. 
V.  Criegern:    Ergebnisse  der  Untersuchung  des  menschlichen  Herzens  mittelst  fluorescir- 

enden  Schirmes,  Verhandl.  d.  Kong.  f.  innere  Med.,  Wiesbaden,  1899,  xvi,  302. 
Rieder,  H.:  Die  Untersuchung  der  Brustorgane  in  verschiedenen   Durchleuchtungsricl - 

tungen,  Fortschr.  a.  d.  Geb.  d.  Rontgenstrahlen,  Hamb.,  1902-03,  y\,  115. 
Moritz,  F.:  Ueber  die  Bestimmung  der  wahren  Grosse  von  Gegenstanden  mittels  des 

Rontgenverfahrens,  Miinchen.   med.  Wchnschr.,  1900,  xlvii,  509,  902.     Ueber  ortho- 

diagraphische  Untersuchungen  am  Herzens,  ibid.,  1902,  xlix,  1.     Ueber  Tiefenbest- 

immungen  mittels  des  Orthodiagraphen  und  deren  Verkiirzungen  bei  der  Orthodia- 

graphie  des  Herzens  zu  ermitteln,  Fortschr.  a.  d.  Geb.  d.  Rontgenstrahlen,  Hamb., 

1904,  vii,  169. 
Levy-Dom:    Schutzmaassregeln    gegen    Rontgenstrahlen    und    ihre    Dosirung,    Deutsche 

med.  Wchnschr.,  Berl.  und  Leipz.,  1903,  xxix,  921. 
For  numerous  forms  of  orthodiagraphs  of  Moritz  and  Albers-Schoenberg  (1.  c),  but  what 

seems  to   the   writer   to   be  the  most  convenient  and  simple  form  is  the  apparatus 

described  by: 
Gillet:  Ein  Orthorontgenograph  einfacher  Konstruction,  Fortschr.  a.  d.  Geb.  d.  Rontgen- 
strahlen, Hamb.,  1906,  x,  114. 


X-RAY   EXAMIXATIOX.  87 

For  the  examination  of  the  heart  cf.  also 

Moritz,  F. :  Einige  Bemerkungen  zur  Frage  der  perkutorischen  Darstellung  der  gesamm- 

ten    Vorderflache   des    Herzens,   Deutsch.  Arch.  f.  khn.  Med.,  Leipz.,  1906,  Ixxxvii, 

276. 
Dietlen,  H.:  Ueber  Grosse  und  Lage  des  normalen  Herzens  und  ihre  Abhangigkeit  von 

physiologischen  Bedingungen,  ibid.,  1906,  Ixxxviii,  55. 
Levy,   M.:  Ueber  Abkiirzung  der  Expositionszeit  hei  Aufnahmen  niit  Rontgenstrahlen, 

Fortschr.  a.  d.  Geb.  d.  Rontgenstrahlen,  Hamb.,  1897,  i,  75. 
Rieder,  H.,  and    Rosenthal,  J.:  Ueber  Moment-Rontgenaufnahmen,  Fortschr.  a.  d.  Geb. 

d.  Rontgenstrahlen,  Hamb.,   1900,  iii,  100. 
Rieder,  H.:  Neue  Ausblicke  auf  die  weitere  Entwicklung  der  Rontgendiagnostik,  Miin- 

chen.  med.  Wchnschr.,  1908,  Iv,  381. 


VI. 

PHYSICAL  EXAMINATION. 

While  it  is  impossible  to  enter  into  a  treatise  upon  physical  exami- 
nation, a  few  points  which  are  of  special  importance  in  cardiac  cases  may 
be  discussed. 

General  Appearance. — The  general  appearance  of  the  patient,  expres- 
sion and  color,  are  of  great  importance.  The  position  which  he  naturally 
assumes  in  bed,  the  presence  or  absence  of  dyspnoea  and  orthopnoea,  the 
general  degree  of  nervousness  or  dulness  are  all  to  be  noted. 

The  typical  appearance  of  the  cardiac  patient  (cardiac  facies)  is 
characterized  by  an  anxious  expression,  bright  eyes  with  moist,  glistening 
conjunctivae,  cheeks  full  rather  than  sunken  as  in  the  abdominal  facies, 
and  as  a  rule  a  tinge  of  cyanosis  about  the  Ups. 

There  are  two  main  types :  (1)  the  mitral  (or  mi  trot  ri  cusp  id)  facies,  with 
rosy,  flushed  cheeks,  dilated  capillaries,  and  cyanosis  (most  conunonly  seen  in  mitral 
stenosis);  and  (2)  the  aortic  facies,  with  pale,  often  sallow,  rather  sunken  cheeks, 
bright  eyes,  moist  conjunctivae,  and  slight  cyanosis  of  Ups  and  fingers.  To  these  might  be 
added  (3)  the  subicteric  facies  of  broken  compensation,  Tvnth  pallor,  subicteric  conjimctivse, 
and  cyanosis  of  the  lips. 

Nasopharynx. — The  tonsils  and  posterior  nasopharynx  should  always  be  carefully 
examined.  The  former  are  the  chief  portals  of  entry  for  the  germs  of  rheumatism,  while 
adenoids  and  affections  of  the  nasal  septum  may  of  themselves  induce 
cardiac  arrhythmia,  and  may  also  be  an  important  contributing  factor  in  the  attacks  of 
asthma  in  organic  heart  disease. 

Ophthalmoscopic  Examination. — The  eye-grounds  should  always  be  examined  when 
arteriosclerosis  (page  260)  or  congenital  heart  disease  (page  438)  is  suspected. 

Neck. — In  the  neck  especial  attention  should  be  directed  to  the  visible 
throbbing  of  the  carotids,  the  fulness  of  the  neck,  and  the  size  and  consist- 
ency of  the  thyroid  gland  (page  585),  the  presence  of  thrills  and  murmurs 
over  vessels  or  thyroid,  or  a  tracheal  tug  (page  533).  The  jugular  pulsation 
is  discussed  in  full  in  Part  I,  Chapter  IV,  page  49. 

Chest. — The  form  of  the  chest  is  of  considerable  importance,  not  only 
as  regards  kyphosis,  but  particularly  as  to  its  fulness  or  flatness  (see 
Part  III,  Chapter  III).  In  recording  this,  the  width  of  the  costal  angle 
should  be  noted,  but  the  general  obliquity  of  the  ribs  in  quiet 
expiration  should  be  designated  by  noting  the  vertebral  spines 
which  are  on  the  same  level  with  the  sternoxiphoid 
articulation  (normally  at  the  level  of  the  eighth  thoracic  spine) 
(page  598).  It  should  be  noted  whether  the  chest  in  quiet  breathing  ap- 
proaches more  nearly  to  the  position  of  expiration,  flat  chest,  or  to  that 
of  inspiration.  Pulsations,  bulgings,  heaving,  or  retractions  of  the  ribs  or 
interspaces,  as  well  as  the  presence  of  abnormal  shocks  and  thrills,  should 
of  course  be  noted. 

Abdomen. — In  the  abdomen  the  important  features  to  be  noted  are 
presence  or  absence  of  ascites,  enlargement  of  liver  (systemic 
88 


PHYSICAL   EXAMINATION.  89 

stasis),  pulsation  of  the  liver,  systolic  impulse  (tricuspid  insuffi- 
ciency), systolic  retraction  (dilated  or  hypertrophied  right  ventricle),  the 
nature  and  the  time  of  epigastric  pulsation  (systolic  elevation  being  trans- 
mitted from  the  abdominal  aorta,  systolic  retraction  indicating  dilated 
hypertrophied  right  ventricle) .  A  palpable  spleen  of  cardiac  origin 
points  to  infarction,  septic  or  thrombotic.  When  aneurism  or  arterio- 
sclerosis is  suspected  the  course  of  the  abdominal  aorta  should 
be  mapped  out  by  deep  palpation  with  both  hands,  one  above  each  side  of 
the  aorta  and  that  vessel  between  them  (page  550) . 

The  genitalia  should  of  course  always  be  examined  for  signs  of  gonor- 
rhoea and  lues, — urethral  smears  for  the  former  and  a  Wassermann 
reaction  for  the  latter  being  made  whenever  possible. 

Extremities. — Upon  the  extremities  the  presence  of  oedema  and 
arthritis,  acrocyanosis  or  pallor,  and  the  size,  consistency,  and 
uniformity  of  the  brachial,  radial,  femoral,  popliteal,  and  dorsahs  pedis 
arteries    are  the  chief  points  of  importance. 

THE    CARDIAC    IMPULSE. 

Mechanics  of  the  Cardiac  Impulse. — The  apex  itself,  as  shown  by 
Ludwig  and  Dogiel,  does  not  move  appreciably  up  or  down  during  systole; 
and,  as  Hesse  has  demonstrated,  the  transverse  diameter  of  the  heart 
shortens  more  than  the  longitudinal. 

The  chief  movements  which  lead  to  the  production  of  the  apex 
impulse  are  due  more  to  the  systolic  erection  of  the  heart  upon  the  great 
vessels  than  to  its  diminution  in  size. 

(  I 

If  one  watches  the  exposed  heart  of  a  dog,  y^ — '     I    "^"-T!'    ~^ — - — \ 

cat,  or  rabbit,  it  is  seen  to  execute  two  move-  y^-   ^^pl^^i^^r~~^)-^  \ 

ments  in  systole:    (1)  the  general   contraction  /.  /Im^^^^     ^wkj         \\ 

affecting  chiefiy  the  transverse  diameter  of  the         /-     /  [1^^^^^^     ^  \  \ 

heart,  and   (2)    a  twisting   about   of   the     Ni./      /    ^^^L    ^\^  \  \ 

apex  from  left  to  right  and  forwards.        /     "i — "^^J /^^^^''=^         ~V    \ 
This  torsion  of  the  apex  is  the  resultant  of  the       /       \  (l      )  /       \ 

several  lines  of  traction  exerted  by  the  muscu-      /         V  /  /  O  ( V  x  \ 

lature  of  the  right  and  left  ventricles  upon  the      1  ^- — -^   \J  ^ — ^  4 

base  of  the  aorta  and  pulmonary  artery,  and       V  ^ 

modified  by  the  pivoting  of  the  heart  against  ^     „.     .,  *     f  »i    i      *  i    j- 

,  •',        ,^  °,         ,         i^T-r-  FiG.So. — Movements  of  the  heart  leading 

the  vertebral  column  and  by  the  shlttmg  of  its  to  the  protrusions  and  retraction  during  sys- 
centre  of  gravity  owing  to  variation  in  its  tele.  Forces  shown  by  the  arrows, 
liquid  content.  The  tendency  of  this  move- 
ment is  to  push  the  apex  of  the  left  ventricle  against  the  chest  wall,  while  the  left 
wall  of  the  left  ventricle  and  the  right  (anterior)  wall  of  the 
right  ventricle  move  inwards  toward  the  septum.  Wherever  in 
man  these  walls  are  in  contact  with  the  chest  wall  these  inward  movements  give  rise  to 
retraction  of  the  interspaces  above  them.  The  surface  of  the  thin-walled  right  ventricle 
moreover  is  actually  pulled  inwards  during  systole,  so  that  there  may  actually  be  an 
indentation  of  its  surface  which  still  further  contributes  to  the  systolic  retraction. 

Protrusions  and  Retractions. — A  variety  of  protrusions  and  retractions 
of  the  interspaces  may  be  seen  to  occur  with  each  cardiac  contraction. 

Graphic  records  of  the  impulse  have  been  taken  by  means  of  the  polygraphs 
described  above,  the  receiving  funnel  being  placed  over  the  area  of  pulsation  exactly 
as   for   a    jugular   or   carotid  tracing.      Tracings  can  be  made   either  with  a  rubber- 


90 


DISEASES   OF   THE    HEART    AND    AORTA. 


covered  spring  tambour  like  that  used  for  the  carotid,  or  with  an  open  funnel  ; 
the  former  exerting  pres&ure  upon  the  apex,  the  latter  merely  recording  the  com- 
pression or  rarefaction  of  the  air  in  the  funnel  due  to  the  impulse. 

The  writer  also  finds  that  a  funnel,  made  from  a  soft  rubber  stethoscope  tip  stoppered 
tightly  with  a  perforated  rubber  stopper  penetrated  by 
a  glass  tube  and  bearing  a  rubber  tip,  is  verv  satis- 
/  factory  (Fig.  86). 

The  movements  seen  may  be  divided  as: 
(1)   Lifting    of   the    entire    precordium. 
which  results,  especially  in  flat-chested  individ- 
uals or  in  those  with   very  large  hearts,  from 
the  systolic  erection  of  the  heart  as  a  whole  as 
it  pivots  against  the  vertebral  column  behind 
and  pushes  against  the  chest  wall  in  front. 
This  is  usually  seen  in  hearts  which  from  any  cause  whatever  are 
beating  heavily,  though  it  is  most  marked  over  large  hearts. 

(2)  The  normal  typo  of  apex  beat  consists  of  a  large  protrusion 
synchronous  with  and  lasting  throughout  the  duration  of  ventricular  systole 
(Fig.  88,  I,  s-d),  usually  preceded  by  a  small  presystolic  wavelet  (as),  due 


Fig.  86. — Rubber  funnel   for  c.ir 
diographic  tracings. 


cd  cd  cd   cd 


cd    cd   cd    cd 


Fio.  87. — A,  tracing  from  the  apex  impulse  and  carotid  artery:  c,  time  of  carotid  wave;  d.  time 
of  dicrotic  notch.  Upper  line  gives  the  time  in  i  sec.  B.  cardiogram  obtained  over  a  normal  apex. 
C  and  D,  cardiogram  over  the  fourth  left  interspaces  cm.  from  costal  margin  (systolic  retraction),  from 
the  same  individual  as  B. 


to  systole  of  the  auricles.  The  large  ventricular  wave  is  followed  by  a  fall 
in  early  diastole,  coincident  with  the  fall  in  intraventricular  pressure. 
After  this  fall  there  is  sometimes  a  small  upstroke  of  the  lever  (passive 
protrusion  of  the  apex  by  the  inrushing  blood)  which  may  terminate  in  a 
small  protodiastolic  wavelet  (p).     This  protodiastolic  wavelet  corresponds 


PHYSICAL  EXAMIXATIOX. 


91 


to  the  shoulder  upon  the  cardiac  plethysmogram  at  the  end  of  ventricular 
filling  (page  9),  and  is  particularly  marked  in  cases  in  which  a  third  heart 
sound  can  be  heard  (Thayer) . 

In  cases  with  hypertrophy  of  the  left  ventricle  the  protrusion  is 
usually  very  forcible  and  heaving  throughout  systole — dome-like  protru- 
sion,  choc  en  dome   (Bard). 

Occasionally,  however,  especially  when  there  is  some  hypertrophy 
of  the  right  ventricle,  the  systolic  protrusion  may  not  last  throughout 
ventricular  systole,  but  may  be  represented  by  only  a  momentary  protru- 
sion, followed  by  a  retraction  during  midsystole  (Fig.  88,  III).  Such  a 
beat,  which  really  represents  the  algebraic  sum  of  the  systolic  protrusion 
over  the  left  ventricle  and  the  systolic  retraction  over  the  right,  may  be 


Fig.  88. — Various  forms  of  apex  tracings.  I.  Normal,  showing  presystolic  (auricular)  wave  a, 
systolic  plateau  s-<l,  and  the  curve  of  ventricular  filling  d-p,  ending  in  the  protodiastolic  wavelet  p.  II, 
Normal  apex  beat  showing  only  systolic  elevation.  III.  "Mixed"  type  of  impulse  showing  an  elevation 
followed  by  a  retraction  during  the  period  of  systole.  IV.  Systolic  retraction.  Apex  formed  by  the 
right  ventricle.  V.  "Mixed"  type  of  apex  beat  showing  protrusion  during  auricular  systole  and 
retraction  during  systole  of  the  ventricle. 


termed  a  "  m  i  x  e  d "  type  of  apex  beat.  In  other  mixed  types 
there  may  be  protrusion  during  auricular  systole  (presystolic  protrusion) 
followed  by  retraction  during  systole  of  the  ventricle  (systolic  retrac- 
tion) .  The  r  i  g  h  t  ventricle  plays  the  leading  role  in  the  production  of 
such  an  impulse. 

(3)  Systolic  retractions  over  the  entire  right  ven- 
tricle (third,  fourth,  fifth  left  interspaces  between  the  parasternal 
line  and  sternal  margin)  when  this  chamber  is  hypertrophied  or 
contracting  strongly,  sometimes  also  in  second  left  interspace 
(Mackenzie).  Occasionally,  especially  in  cases  of  mitral  stenosis,  the 
presence  of  a  systolic  retraction  of  the  interspaces  over  the  right  ventricle 
and  a  systolic  protrusion  over  the  apex  gives  the  cardiac  impulse  the 
w  a  V  y  appearance  of  a  peristalsis.  In  reality,  however,  the  two  move- 
ments are  synchronous.     It  is  not  a  peristalsis  but  a  see-saw  movement. 


92 


DISEASES   OF   THE   HEART    AND    AORTA. 


(4)  Systolic  impulse  in  the  second   right  interspace  in  aortic 
insufficiency. 

(5)  Systolic  impulse  in  the  second  left  interspace  (pulmonic  area)  in 
pulmonary  insufficiency  or  vigorous  contraction  of  the  right  ventricle. 


(6)    Systolic     retraction    at 


Fig.  89. — Areas  of  pulsation  and  retraction.  •  , 
protrusion;  i  ,  retraction.  CAR,  carotid  artery;  JUG, 
jugular  vein;  CEPH,  cephalic  vein;  AO,  aorta;  PA,  pul- 
monary artery;  RV,  right  ventricle;  APHD,  apex  with 
high  diaphragm;  AP,  apex;  LIV.TR.INS,  liver-pulsa- 
tion in  tricuspid  insufficiency;  LIV .  HYP.  RV,  liver- 
retraction  with  hypertrophy  of  right  ventricle. 


the  apex  in  adherent  peri- 
cardium or  when  the  apex  is 
formed  by  an  hypertrophied 
right  ventricle. 

(7)  Systolic  retrac- 
tions in  the  interspaces 
beyond  the  apex  (left  axilla)  due 
to  negative  pressure  over  those 
areas  of  lung  produced  by  con- 
traction of  a  very  large  heart  or 
to   pleuropericardial    adhesions. 

(8)  Retraction  of  the 
xiphoid  process  or  ribs 
from  traction  of  costopericardial 
adhesions  during  systole 
(Broad bent's   sign). 

(9)  Systolic  impulses 
in  various  abnormal  sites 
due  to  aneurisms,  tumors,  or 
tortuous   sclerotic    arteries. 


PALPATION. , 

Palpation  of  the  precordium  and  thorax  is  undertaken  with  a  view 
to  determine,  O)  the  force  of  the  apex  impulse;  (2)  the  presence  and  force 
of  any  diffuse  heave;  (3)  the  intensity  of  the  shock  accompanying  the 
heart  sounds;  (4)  the  presence  and  distri-  !     * 

bution  of  "thrills";    (5)  the  presence,  dis-  \ 

tribution,  and  character  of  other  pulsations. 

Thrills. — Corrigan  (1837)  and,  later,  Marey 
showed  that  thrills  may  be  imitated  by  producing  a 
constriction  in  a  rubber  tube  attached  to  a  water 
faucet.  It  will  be  seen  that  this  causes  the  stream  to 
assume  a  corkscrew  form,  giving  rise  to  eddies,  twists, 
and  nodes  below  the  constriction.  These  tend  to  produce  zones  of  constriction  and  dilatation 
in  the  tube  itself  and  thus  set  it  into  vibrations  which  are  palpable  as  thrills  and  audible  as 
murmurs.    Above  the  constriction  there  are  no  eddies,  hence  neither  thrills  nor  murmurs. 

The  thrill  is  best  transmitted  in  the  direction  of  the  stream  producing 
it.  It  disappears  when  the  constriction  becomes  too  great  or  the  pressure 
falls  too  low,  and  increases  with  the  force  of  the  stream  (blood-pressure). 


Fig.  90. — Eddies  producing  thrills  as 
illustrated  by  a  stream  of  water.  Arrows 
show  lines  of  force.  The  large  arrow  indi- 
cates the  pressure  at  the  point  of  palpation. 


PERCUSSION. 

It  is  of  the  greatest  importance  to  determine  the  exact  outline  of  the 
heart.  As  has  been  seen,  this  is  done  most  accurately  by  means  of  the 
orthodiagraph  (page  85),  but  under  ordinary  clinical  conditions  this  is 
not  available  and  the  cardiac  area  is  outlined  by  percussion. 


PHYSICAL   EXAMINATION.  93 

In  determining  the  area  of  cardiac  dulness  it  is  important  to  map  out, 
(1)  the  area  of  cardiac  dulness,  or,  more  accurately,  the  relative  cardiac 
dulness;  (2)  the  area  of  absolute  dulness  or  cardiac  flatness. 

RELATIVE    CARDIAC    DULNESS. 

In  mapping  out  the  area  of  relative  cardiac  dulness  it  is  important 
to  begin  percussion  as  far  away  from  the  heart  as  possible,  and  then  to 
approach  the  heart,  marking  the  points  at  which  the  very  first  change  of 
note  can  be  recognized  as  the  heart  is  approached.  In  this  way  one  obtains 
an  absolutely  resonant  note  as  long  as  the  plessimeter  finger  is  over  lung 
tissue,  and  a  sharp  contrast  to  this  as  soon  as  one  percusses  over  the  borders 
of  the  heart;  whereas,  if  one  were  to  begin  percussion  over  the  heart  and 
percuss  outward  there  would  be  a  gradual  change  of  note, 
becoming  more  and  more  resonant,  until  it  finally  faded 
into  the  perfect  resonance  over  the  lung.  ^^r\^ 

Choice  of  Methods. — In  outlining  the  cardiac  area  one  has  the 
choice  of  several  methods: 

(1)  Direct   or  immediate  percussion  by  tapping  the  chest  wall 
directly  with  the  finger-tips  of  one  hand. 

(2)  Heavy   indirect  or  mediate  percussion. 

(3)  M  e  d  i  u  m  - 1  i  g  h  t   percussion. 

(4)  Lightest    audible    percussion    (threshold    percussion   of 
Ewald,  Goldscheider,  Curschmann  and  Schlayer).  ^* 

(5)  Palpatory  percussion  (Ebstein)  by  note  too  low  to  be  Fig.  91. — Gold- 
heard  at   all.                                                                                                                                    scheider's  ortho- 

(6)  Orthopercussion     (Goldscheider)    (Fig.    91),   distal      Percussion. 
phalanx  of  the  plessimeter  finger  held  perpendicular  to  the  chest  wall. 

(7)  Instrumental  percussion  with  a  mechanical  plessimeter,  the  blow  being 
struck  by  either  the  finger  or  a  hammer. 

In  selecting  the  method  of  percusvsion  it  should  be  borne  in  mind  that, 
though  bodies  near  the  chest  wall  on  either  side  of  the  line  of  percussion 
stroke  may  tend  to  damp  the  vibration  of  the  lung  and  impair  the  reso- 
nance of  the  note,  this  tendency  is  greater  for  heavy  percussion  and  loud 
resonance  than  with  light  strokes  which  set  only  small  areas  of  lung  in 
vibration.  Moreover,  it  is  a  well-known  law  of  sense-perception  that  the 
softer  the  initial  sound  the  easier  it  is  to  detect  variations  in  it.  Indeed, 
de  la  Camp  goes  so  far  as  to  recommend  light  direct  percussion  through  a 
single  layer  of  blanket  laid  upon  the  chest  as  the  most  accurate  method 
of  outlining  the  cardiac  dulness. 

Moritz,  Dietlen,  de  la  Camp,  Goldscheider,  Curschmann  and  Schlayer, 
and  a  number  of  other  writers  have  compared  outlines  made  by  the  various 
methods  of  percussion  in  hundreds  of  cases  with  those  obtained  by  the 
orthodiagraph,  while  Simon  has  marked  out  his  outlines  by  percussion 
upon  the  intact  cadaver  with  pins  and  then  tested  his  accuracy  upon 
opening  up  the  thorax.  All  these  observers  are  unanimous  in 
advocating  very  light  percussion  for  outlining  the  left  border 
of  the  heart,  but  Moritz  prefers  a  rather  heavy  palpatory  percussion 
for  the  right  border. 

Moreover,  the  sensations  which  percussion  imparts  to  the  finger  are 
more  delicately  graded  for  a  light  stroke  than  for  a  heavy  one,  since  the 


94 


DISEASES   OF   THE   HEART    AND   AORTA. 


pressure  of  a  heavy  blow  somewhat  dulls  the  sensibility  of  the  finger-tips, 
and  in  this  way  also  a  light  stroke  is  more  satisfactory.  The  oft-made 
claim  that  a  light  stroke  does  not  penetrate  deep  enough  for  mapping  out 
the  right  border  of  the  heart,  though  seeming  plausible,  is  not  warranted  by 
experience.  On  the  contrary,  the  writer  has  observed  that  those  clinicians 
who  rarely  make  out  at  all  the  area  of  cardiac  dulness  which  lies  to  the 
right  of  the  midline  were  usually  those  who  used  heavy  percussion. 

Avoidable  Errors  in  Percussion. — The  exact  method  used  is  a  matter  of  individual 
preference  and  practice.  The  essentials  for  all  forms  are:  (1)  a  loose  wrist,  loosely  held 
finger-joints,  and  a  short  sharp  blow  with  immediate  elastic  recoil;'  (2)  firm  pressure  of 
the  plessimeter  finger  against  the  chest  wall,  especially  in  the  interspaces.  In  the  writer's 
experience  the  important  point  is  not  the  method  used  but  the  care  in  discriminating  the 
first  slight  differences  in  note  and  sensation.  The  errors  of  percussion  so  frequent  among 
students  and  even  experienced  physicians  are  far  more  frequently  due  to  in- 
ability to  detect  differences  in  note  than  to  inability  to  elicit 
them.  This  inability  to  detect  slight  differences  was  due  in  most  cases  to  a  precon- 
ceived notion  as  to- the  intensity  of  change 
obtainable.  The  observer  usually  expected  a 
greater  change  and  permitted  his  ear  to  neglect 
the  lesser,  although  once  his  attention  was 
called  he  was  perfectly  able  to  detect  it. 

Special  Methods  of  Percussion.^ — The 
method  of  choice  varies  somewhat  with  the 
purpose.  For  ordinary  purposes  very  light 
direct  percusf;ion  is  quite  satisfactory,  or  ordi- 
nary threshhold  percussion  with  barely  audi- 
ble note.  Where  accuracy  is  important, 
as  in  determining  the  mobility  of  the  heart 
or  of  the  lung  borders,  Goldscheider's  or- 
thopercussion or  J.  O.  Hirschfelder's 
orthoplessimeter    is   preferable. 

Goldscheider  beUeved  that  orthopercus- 
sion was  so  delicate  that  dulness  was  given 
only  by  bodies  directly  in  the  axis  of  the 
plessimeter  phalanx  and  that  in  this  way  the 
plane  of  an  oblique  surface  could  be  detected;  but  experience  shows  that  this  is  rarely 
possible.  It  succeeds  much  more  frequently  when  the  orthoplessimeter  (Fig.  92)  is 
used;  so  that  a  resonant  note  may  be  obtained  when  the  shaft  is  pointed  parallel  to  the 
heart  surface,  a  dull  note  when  it  is  pointed  toward  the  heart. 

Unavoidable  Errors  in  Percussion  Outlines. — In  outlining  the  heart 
by  percussion  the  right  and  left  borders  present  different  problems.  The 
right  border  is  situated  deeply  and  recedes  at  once  from  the  chest  wall,  so 
that  it  represents  the  first  point  at  which  dulness  could  be  obtained.  The 
left  border  is  superficial  and  convex  and  the  convexity  sometimes  follows 
the  curve  of  the  ribs  in  the  left  axilla.  Accordingly  it  may  happen  that  in 
round  narrow  chests  or  in  persons  with  large  hearts  the  left  ventricle  may 
almost  fill  the  left  half  of  the  thorax.    The  curve  of  the  ribs  follows  the  wall 


Fig.  92. — Percussion  with  the  orthoplessi- 
meter. A.  J.  O.  Hirschfelder's  orthoplessimeter 
and  its  mode  of  application.  B.  Supposed  line  of 
transmission  of  the  percussion  impulse  from  the 
orthoplessimeter.    RES,  resonant  percussion  note. 


*  Some  persons  are  possessed  of  a  loose  wrist  at  once,  others  acquire  it  only  after 
long  practice.  For  the  latter  the  writer  recommends  the  following  exercise  practised  two 
to  five  minutes  daily:  Hold  the  wrist  as  loosely  as  possible,  then  vibrate  the  forearm  very 
rapidly  to  and  fro  from  the  elbow  until  the  hand  shakes  about  like  a  Hail  upon  the  loose 
wrist  too  fast  for  the  eye  to  follow  its  movements.  The  improvement  in  percussion  fol- 
lowing this  exercise  is  very  gratifying. 


PHYSICAL   EXAMINATION. 


95 


of  the  left  ventricle  and  the  latter  may  remain  near  the  chest  wall  through- 
out the  axilla.    The  outer  border  of  dulness  may  thus  be  obtained  not  over 
the  apex  but  over  the  posterior  wall  of  the  left  ventricle.     In    persons 
with    narrow    chests    or    much 
enlarged    hearts    the    area    of 
dulness    (Fig.    93,    P P)    ex- 
tends    around     the     heart     and 
not    merely    across    the    trans- 
verse   diameter    (O O).      The 

transverse  diameter  ( O O )  corre- 
sponds accurately  to  the  point  mapped 
out  with  the  orthodiagraph.  Accord- 
ingly there  may  be  a  discrepancy  of 
several  centimetres  between  the  percus- 
sion and  orthodiagraph  estimations  of 
the  distance  from  the  midline  to  the 
left  border.  In  broad  flat  chests  where, 
beyond  the  apex,  the  left  ventricle  recedes 

from  the  chest  wall,  this  discrepancy  does  not  occur;  and  the  findings  by 
percussion  and  by  X-ray  coincide  closely.  In  a  very  large  series  of 
cases  Moritz  found  his  percussion  (light  percussion  for  the  right  border, 
threshold  percussion  for  the  left)  to  be  correct  for  the  right  border  in 
86  per  cent.,  for  the  left  in  70  per  cent. 


Fig.  93. — Diagram  to  show  the  cause  of 
unavoidable  error  in  percussion  of  the  cardiac 
outlines.  P  —  P,  outline  on  percussion; 
O  —  O  orthodiagraph  outUne. 


DIAMETER    OF    THE    CARDIAC    AREA. 

In  mapping  out  the  area  of  cardiac  dulness  the  position  of  the  apex  is 
given,  designating  the  level  of  rib  or  interspace  during  quiet  respiration,  and 

the  number  of  centimetres  to 
the  left  of  the  midline  (Figs.  84 
and  94)  (.ML).  The  level  of 
upper  border  at  the  left  sternal 
margin  is  giyen  and  also  the 
distance  to  the  right  of  the 
midline  (MR)  in  the  fourth 
right  interspace.  The  acuteness 
or  obtuseness  of  the  angle 
formed  between  the  hepatic  and 
the  cardiac  dulness  (cardio- 
hepatic  angle,  angle  of  Ebstein) 
is  also  noted.  In  addition  to 
this  Moritz  and  Dietlen  call 
attention  to  the  importance  of 
'recording  the  two  diagonal  di- 
ameters of  the  heart  (longitu- 
dinal, L,  from  apex  to  the 
aortic  angle  of  the  dulness,  and  transverse,  Q,  from  the  cardiohepatic 
angle  to  the  upper  left  border,  as  shown  in  Fig.  84).  Normal  figures  for 
these  conjugates  according  to  Dietlen  are: 


Fig.  94. — Areas  of  cardiac  dulness  and  flatness  in  a 
normal  man.  The  outer  fine  line  represent*  cardiac  dul- 
ness; the  inner  heavy  line  represents  cardiac  flatness. 


96 


DISEASES    OF   THE    HEART    AND    AORTA. 


Height  of  individual. 

Men. 

Women. 

Cm. 

Feet  and  In. 

MR.        ML.          L. 
Cm.         Cm.        Cm. 

Q       i  Cardiac 
Qcm. 

MR. 
Cm. 

ML. 
Cm. 

L. 
Cm. 

Cm. 

Cardiac 
area. 
Qcm. 

145-154 
155-164 
165-174 
175-187 

4.7—5. 
5.1—5.5 
5.5—5.9 
5.9—6.2 

3.5 
4.1 

4.2 
4.4 

7.9 
8.7 
8.8 
9.1 

12.5 
13.8 
14.1 
14.8 

9.7         95 

9.9       109 

10.3       116 

10.7       127 

3.5 
3.5 
3.8 

8.1 
8.4 
8.5 

12.7 
13.2 
13.4 

9.4 

9.7 
9.9 

93 
101 
105 

Dulness  in  Children. — In  children  the  heart  is  proportionately  larger  and  lies  more 
transversely  than  in  adults.  The  apex  is  usually  in  the  fourth  interspace  lateral  from  the 
nipple.  Veith  has  shown  that  the  cardiac  shadow  in  children  extends  exactly  twice  as 
far  to  the  left  as  to  the  right  of  the  midline  (ML  :  MR  2:1). 

Changes  in  the  Relative  Dulness. — The  relative  proportions  of  the 
various  conjugates  undergo  quite  typical  changes  in  various  forms  of  heart 

disease.  In  weakening  of  the  right 
heart,  in  tricuspid  insufficiency,  and 
tricuspid  stenosis  the  conjugate  MR  is 
increased  (dulness  increased  to  the 
right) ;  in  hypertrophy  of  the  left  ven- 
tricle and  in  mitral  insufficiency,  dulness 
increases  to  the  left  (MR  increased), 
while  in  the  latter  condition  as  well  as 
in  mitral  stenosis  the  oblique  transverse 
diameter  (Q)  is  increased.  In  aortic 
disease  there  is  lengthening  of  the 
long  axis  (L). 

CARDIAC    FLATNESS. 


Fig.  95.  —  Cardiac    outlines   in 
nine  years. 


The    area    of    absolute    dulness    or 

child  of     cardiac  flatness  represents  the  portion 

of  the  heart  which  is  not  covered  by 

lung    (Figs.  93    and    94).      It    forms  a 

triangle  extending  from  the   fourth  rib  above  to  within  2-3  cm.  of  the 

apex,   or  even  just  to  the  latter  in  the  fifth  left  interspace. 

It  is  best  mapped  out  by  very  light  percussion,  beginning  over  in  the 
fifth  left  interspace  at  the  left  sternal  margin,  percussing  lateral  ward 
and  upward,  passing  from  the  absolute  flatness  to  the  area  of  impaired 
resonance  instead  of  in  the  opposite  direction). 

Variations  in  the  Area  of  Flatness. — In  the  primitive  mammals  (dog, 
cat,  rabbit)  the  heart  does  not  lie  in  close  apposition  to  the  chest  wall,  but 
is  slung  rather  loosely  between  the  folds  of  the  mediastinum  and  com- 
pletely covered  by  lung.  There  is  no  area  of  flatness.  This  same  condition 
is  met  with  in  many  otherwise  normal  persons,  especially  in  the  long  flat- 
chested,  and  in  those  who  have  extremely  movable  hearts  or  general  mo- 
bility of  all  the  viscera  (visceroptosis,  enteroptosis,  page  598). 

Entire  absence  of  cardiac  flatness  is  also  found  in  the  exact 
opposite  type  of  chest,  in  the  barrel-chest  patients  with  emphysema,  in 


PHYSICAL   EXAMINATION. 


97 


whom  the  exaggerated  efforts  at  inspiration  have  caused  the  lungs  to  be 
sucked  in  gradually  between  the  heart  and  the  chest  wall. 

On  the  other  hand,  the  area  of  cardiac  flatness  is  often 
enlarged  in  persons  with  flat,  rhachitic,  or  tuberculous  chests.  In 
hypertrophy  of  the  right 
ventricle  the  area  of  flatness 
is  enlarged  and  the  right  border 
becomes  oblique,  extending 
downward  to  the  right  margin 
of  the  sternum,  often  interrupted 
by  step-like  protrusions  (Kroe- 
nig).  In  pericardial  effusion  it 
extends  well  into  the  fifth  right 
interspace. 

Changes  in  Size  of  the 
Heart. — As  seen  in  the  investi- 
gations upon  cardiac  volume, 
the  size  of  the  heart,  and  hence 
the  area  of  cardiac  dulness,  is 
subject  to  a  physiological  in- 
crease when  the  heart  is  slow 
and  decrease  in  size  when  it  is 
rapid  (Henderson,  see  page  9). 
This  decrease  in  size  is  especially 
noticeable  in  certain  cases  with 
rapid  hearts,  like  paroxysmal 
tachycardia  when  there  is  no 
heart  failure  nor  vasodilation 
(Hoffmann,  Dietlen).  An  in- 
crease in  size  may  be  associated 
with  a  slow  pulse  (see  page  9 
and  Fig.  12),  hypertrophy  of 
the  heart,  or  with  a  pathological 
dilatation.  The  physiological 
condition  should  first  be  con- 
sidered before  assuming  the 
pathological. 

Changes  in  Position  of  the 
Heart. — (1)  Upon  changes  in 
posture.  Normally  changes 
in  posture  are  accompanied  by 
considerable    changes    in    the 

position  of  the  heart.  The  apex  may  move  3-5  cm.  when  the  patient 
turns  from  one  side  to  the  other,  always  moving  towards  the  side  which 
is  lower.  On  standing  a  similar  but  less  marked  change  occurs.  Moritz, 
and,  later,  Dietlen  have  shown  that  the  area  of  the  cardiac  shadow  is  from 
ten  to  thirty  per  cent,  smaller  on  standing  than  on  lying  down.  The  latter 
observer  confirms  Erlanger  and  Hooker  in  stating  that  the  pulse-pressure, 
and  hence  the  systolic  output  of  the  ventricles,  diminishes  correspondingly. 
7 


Fig.  96. — Diagrams  illustrating  the  movements  of 
the  normal  heart  on  change  of  posture  from  side  to  side 
(A),  and  in  the  various  phases  of  respiration  (B).  Solid 
black  line,  normal  cardiac  outline  in  quiet  breathing; 
dotted  line  (R),  cardiac  outline  with  patient  lying  on 
right  side;  broken  line  (L),  cardiac  outline  with  patient 
lying  on  left  side;  EXP  (horizontal  shading),  outline  in 
expiration;  INSP  (vertical  shading),  cardiac  outline  in 
inspiration.  The  movements  shown  in  tliese  figures 
represent  the  upper  limits  of  normal  mobility. 


98  DISEASES   OF   THE   HEAI?T   AND    AORTA. 

The  diminished  filling  of  the  heart  is  due  also  to  the  fact  that  the  pressure 
under  which  the  blood  enters  it  in  diastole  (venous  pressure)  is  lower  upon 
standing  than  upon  lying  down. 

In  some  people  extreme  mobility  (6-8  cm.)  of  the  apex  is  found  (wan- 
dering heart)— a  condition  often  associated  with  cardiac  neurasthenia 
and  palpitation,  and  even  paroxysmal  tachycardia.  Changes  in  position 
of  the  diaphragm,  upon  expiration,  inspiration,  or  intestinal  flatulence,  also 
affect  the  position  of  the  heart,  especially  upon  standing;  so  that  in 
expiration  or  flatidence  the  apex  is  pushed  up  and  the  heart 
lies  more  transversely,  while  in  inspiration  the  apex  falls  and 
the  heart  lies  more  nearly  in  the  long  axis  of  the  body  (Fig.  96).  As  can 
be  readily  shown  with  Henderson's  cardiometer,  the  former  position  inter- 
feres with  the  cardiac  filling  and  hinders  the  circulation,  while  the  latter 
position  facilitates  both.  The  amount  of  change  of  position  of  the  apex 
is  normally  about   1-2  cm. 

AUSCULTATION. 

CHARACTER    AND    TIME    OF    THE    HEART    SOUNDS. 

The  beat  of  the  heart  is  accompanied  by  two  definite  sounds  ordinarily 
likened  to  the  syllables  "lub-dub"  or  "ta  ta,"  the  first  sound  accompany- 
ing systole,  the  second  occurring  just  at  the  beginning  of  diastole. 

Graphic  Records. — The  exact  period  of  the  cardiac  cycle  to  which  they  correspond 
was  first  investigated  by  Bonders  (1856),  who  marked  the  onset  of  the  sounds  by  tapping 
upon  a  receiving  tambour  the  instant  he  heard  sound  and  recording  this  signal  upon  a  drum 
while  simultaneously  recording  the  cardiogram.  This  method  was  subsequently  developed  by 
Martius  and  has  furnished  some  interesting  information,  but  even  in  regular  pulses  the  results 
are  very  fallible  and  the  method  cannot  be  used  at  all  when  the  pulse-rate  is  irregular. 


CAROTID  L 


PHONOGRAM 


Fig.  97. — Graphic  records  of  the  heart  sounds.     (Kindness  of  Prof.  Einthoven.)    Each  vertical  division 

represents  .02  sec. 

During  the  past  fifteen  years  several  methods  of  recording  the  heart  sounds  graphi- 
cally have  been  devised  (Einthoven  and  Geluk,  Huerthle,  Holowinski).  Einthoven, 
Flohil,  and  Battaerd  place  a  microphone  over  the  heart,  connect  the  microphone  with  the 
thread  galvanometer,  and  photograph  the  movements  of  the  latter. 

O.  Frank  attaches  the  tube  of  a  stethoscope  to  a  tambour  over  which  there  is 
stretched  a  delicate  condom  membrane  bearing  a  small  mirror.  A  beam  of  light  is  thrown 
upon  this  mirror,  and  its  movements,  coincident  with  the  sound  waves  in  the  stethoscope, 
are  recorded  photographically. 

A  still  more  delicate  method  is  that  of  Weiss  and  Joachim.  Instead  of 
the  condom  membrane  used  by  Frank,  these  investigators  register  the  vibrations  of  a  soap 
bubble  film  blown  over  their  receiving  tambour.  To  prevent  bursting  this  is  kept  in  a 
moist  chamber  of  glass.  The  vibrations  are  magnified  by  means  of  a  small  L  of  glass  cap- 
illary which  rests  upon  the  film.  The  movements  of  the  shadow  cast  by  the  end  of  the  L 
are  recorded  photographically.    Weiss  and  Joachim's  results  are  at  least  as  good  as  those 


^"  PHYSICAL   EXAMINATION.  99 

^^ 

of  Einthoven.  Their  records  are  similar  and  quite  as  delicate,  and  add  much  to  our  knowl- 
edge of  heart  sounds.  Moreover,  they  are  able  actually  to  synthetize  and  reproduce  these 
sounds  by  transferring  their  curves  to  zinc  strips  which  are  rotated  upon  a  drum  and  set 
a  stile  in  motion.  The  vibration  gives  rise  to  sounds  which  they  state  have  been  identified 
by  other  clinicians  with  those  of  the  cases  recorded. 

Several  methods  of  recording  the  heart  sounds  by  vibrations  of  a  gas  flame 
(Marbe,  Roos)  have  been  only  moderatelj'  successful,  and  though  simple  are  not  as 
satisfactory  as  the  photographic  methods. 

Clinical  Diagram  for  Heart  Sounds. — In  many  text-books  the  heart 
sounds  are  represented  graphically  in  various  ways,  but  it  seems  to  the 
writer  that  the  best  is  to  indicate  the  occurrence  of  the  sounds  directly 
upon  a  simple  diagram  which  indicates  the  relation  to  the  auricular  and 
ventricular  contractions,  as  shown  in  Fig.  98.' 


CARDIAC  CYCLE 
HEART  SOUNDS- 


^j~\ y^r\ 


1  2  1 


Fig.  98. — Diagram  for  representing  the  heart  sounds  in  clinical  notes.  Upper  curve  represents 
the  events  of  the  cardiac  cycle,  the  small  auricular  contraction  followed  by  the  larger  ventricular  con- 
traction. Lower  line  represents  the  heart  sounds.  True  heart  sounds  are  represented  by  solidly  shaded 
blocks,  whose  height  indicates  their  intensity  and  whose  breadth  indicates  their  duration.  • 

CAUSES    OF    THE    HEART    SOUNDS. 

First  Sound. — Harvey  states  that  "when  there  is  the  delivery  of  a 
quantity  of  blood  from  the  veins  to  the  arteries,  a  pulse  takes  place  which 
can  be  heard  within  the  chest."  Laennec  (1819)  was  the  first  to  describe 
the  character  of  the  sounds.  He  regarded  the  first  sound  as  due  to  ventric- 
ular systole,  though  he  thought  the  second  to  be  due  to  the  contraction 
of  the  auricle.  In  1836,  C.  J.  B.  Williams  and  a  committee  of  the  British 
Medical  Association  investigated  the  heart  sounds  experimentally.  He 
believed  that  the  first  sound  was  largely  of  muscular  ori- 
gin, like  the  contraction  sound  of  skeletal  muscles,  because  it  could  be 
heard  upon  the  excised  heart  even  when  the  auriculoventricular  valves 
were  held  open  with  the  fingers,  but  the  second  sound  could  not  be  heard 
unless  the  aortic  or  pulmonic  valves  closed.  This  view  was  substantiated 
by  Ludwig  and  Dogiel;  but  Sibson  and  Broadbent  found  that  in  the  exposed 
heart  of  the  ass  the  first  sound  begins  with  a  sort  of  rumble,  which  disap- 
pears when  the  blood  flow  is  shut  ofT  by  tying  the  venae  cava?.  This 
rumble  they  ascribe  to  the  movement  of  the  auriculo- 
ventricular  valves. 

Graphic  records  of  the  heart  sounds  by  Einthoven,  Flohil,  and  Battaerd 
have  shown  that  the  first  sound  in  man  begins  at  the  beginning  of  ven- 
tricular systole  and  lasts  .07  to  .10  sec.  It  is  loudest  at  its  very 
beginning,  is  decrescendo  in  character,  and  is  almost 
completed  before  the  aortic  valves  open, — i.e.,  before  the 
heart  has  begun  to  pump  blood  into  the  aorta.    The  first  sound  is  followed 


^Thus  in  cases  of  mitral  stenosis  (see  page  348)  the  first  sound  may  be  short  and 
tapping  in  character,  though  tracings  show  the  systole  to  be  of  duration  no  less  than  that 
met  with  in  the  absence  of  tapping  character  (Hirschf elder). 


100  DISEASES    OF   THE   HEART   AND    AORTA. 

by  the  short  pause,  which  usually  lasts  .15  to  .25  sec,  and  which  is  then 
followed  by  the  second  sound.  Einthoven's  results  have  been  confirmed 
in  man  by  the  records  of  Weiss  and  Joachim,  Hess  and  Frank,  as  well  as 
by  Prof.  Barker,  Dr.  Bond,  and  the  -writer.  In  the  dog,  R.  H.  Kahn  has 
shown  that  the  duration  of  the  first  sound  is  exactly  coincident  with  the 
period  during  which  the  intraventricular  pressure  is  rising,  while  the  dura- 
tion of  the  short  pause  is  exactly  coincident  with  the  systolic  plateau. 

Sahli  and  other  clinical  observers  believe  that  the  first  sound  at  the 
aortic  area  begins  later  than  that  at  the  apex  and  is  due  to  the  rush  of 
blood  from  the  ventricle  into  the  aorta,  but  graphic  records  seem  to  indicate 
that  the  sounds  in  the  two  areas  are  synchronous,  and  begin  before  the 
aortic  valves  open. 

However,  the  first  sound  heard  on  listening  in  the  suprasternal  notch 
is  often  split;  and  it  is  possible  that  the  latter  portion  of  this  sound  is  due 
to  just  such  a  forcible  distention  of  the  aorta. 

The  valvular  element  of  the  sound  is  probably  brought  about  when 
the  valves  are  thrown  into  tension  by  the  ventricular  systole.  The  normal 
valves  give  no  sound  at  all  when  they  open  spontaneously.'  There  is  no 
evidence  to  indicate  that  the  normal  sound  is  brought  about  to  any  extent 
by  eddy  currents  as  are  thrills  or  murmurs,  nor  does  systole  of  the  auricles 
produce  any  portion  of  the  normal  first  sound  (Einthoven). 

Hess  and  Frank  believe  that  the  movement  of  the  heart  within  the 
chest  and  perhaps  against  the  chest  wall  (systolic  erection)  may  be  an 
important  factor  in  the  production  of  the  first  sound.  This  might  explain 
why  the  heart  sounds  are  occasionally  inaudible  in  emphysematous  per- 
sons in  whom  the  organ  is  separated  from  the  chest  wall  by  a  layer  of  lung. 
On  the  other  hand,  this  factor  is  shown  to  play  only  a  minor  role  by  the 
fact  that  the  first  sound  may  be  heard  in  its  normal  intensity  in  the  exposed 
and  even  the  suspended  dog's  heart. 

Second  Sound. — The  second  sound  has  been  shown  by  C.  J.  B.  Williams 
and  the  British  Commission  to  accompany  the  closure  of  the  aortic  and 
pulmonary  valves,  to  be  modified  w^hen  these  valves  arc  injured,  and  to  dis- 
appear when  they  are  held  against  the  vessel  wall.  It  lasts  about  .05  second. 
It  is  loudest  when  the  blood-pressure  is  high,  when  the  valves  are  thicker 
and  more  rigid  than  normally,  or  when  the  vessel  walls  are  more  elastic 
than  usual,  the  intensity  varying  at  different  times  of  life  and  under  patho- 
logical conditions. 

METHODS    OF    AUSCULTATION. 

Monaural  Stethoscope. — The  monaural  stethoscope,  introduced  by 
Laennec,  is  a  simple  wooden  tube  surmounted  by  a  flat  disk  acting  as  an 
ear-piece  and  resonator.  The  tube  is  pressed  against  the  chest  and  the  ear 
laid  upon  the  disk,  so  that  the  observer  receives  at  once  the  sound  and  the 
thrill  in  the  wood  transmitted  directly.  Obviously  this  method  accentuates 
the  notes  of  low  pitch  which  are  nearest  to  the  essential  tone  of  the 
instrument  (and  constitute  most  of  the  normal  sounds),  as  well  as  those 

'  Both  the  valves  and  the  cardiac  walls  are  at  that  time  extremely  lax  and  the  val- 
vular opening  is  almost  equal  to  the  diameter  of  the  ventricular  chamber. 


PHYSICAL   EXAMINATION.  101 

of  relative  loudness,  which  cause  it  to  vibrate  mechanically.  Hence  it 
is  particularly  adapted  to  the  detection  of  presystolic  and  other  rum- 
bling murmurs,  and  is  the  method  used  almost  exclusively  outside  of  the 
United  States. 

Binaural  Stethoscope. — In  the  United  States  the  binaural  stethoscope 
is  in  more  general  use.  This  consists  essentially  of  a  small  receiving  bell 
which  is  placed  upon  the  chest  wall,  and  from  which  two  tubes  lead  off  to 
small  rubber  ear-pieces  which  fit  tightly  into  the  external  auditory  meatus. 
The  most  important  essentials  in  these  three  forms  are,  (1)  a  bell  composed 
of  various  materials — ivory,  wood,  celluloid,  or  hard  rubber — provided  with 
a  sufficiently  large  air  space  at  the  tip  (Emerson) :  (2)  ear-pieces  perfectly 
fitting  the  ear  of  the  individual.  It  is  safe  to  say  that  more  errors  of  auscul- 
tation result  from  poorly  fitting  ear-pieces  than  from  real  inefficiency  on 
the  part  of  the  listener.  (3)  In  stetho- 
scopes in  which  the  ear-pieces  are  held  ! 
in  the  ears  by  a  spring  this  should  not 
exert  excessive  pressure  lest  it  produce 
sounds  within  the  ear  from  the  pressure 
on  the  drum. 

There  are  three  main  forms  of  binau- 
ral    stethoscope:      (1)     those     with     rigid  Fig.  99.— Choice  of  stethoscope  bells. 

tubes   (Gannett's),  (2)   those   with   soft 

rubber  tubes,  (3)  those  with  soft  rubber  tubes,  flat  bells,  and  a  small  elastic 
disk  of  metal  or  celluloid  to  act  as  a  resonator  (Bowles).  Of  these  three 
forms  it  may  be  said  that  the  rigid  tubes  certainly  convey  the  sounds  some- 
what better,  but  this  is  often  more  than  compensated  for  by  the  better 
fitting  of  the  ear-pieces  in  stethoscopes  with  soft  rubber  tubes.  In  steth- 
oscopes with  disks  certain  sound  waves,  and  particularly  those  of  high  pitch 
(soft  blowing  murmurs),  are  accentuated,  while  other  sounds  may  be  rela- 
tively suppressed.  Moreover,  any  movement  of  skin  or  hair  over  the  disk 
may  give  rise  to  a  sound  simulating  a  friction,  and  this  source  of  error 
must  be  carefully  excluded.  Hair  should  be  moistened,  and  a  small  bell 
should  be  used  with  perfect  approximation  to  the  skin  throughout  its 
circumference. 

Alteration  of  Sounds  by  Pressure. — Emerson  has  shown  that  many 
murmurs,  especially  presystolic  and  snapping  sounds,  are  diminished  or 
obliterated  by  pressure  with  the  stethoscope,  while  certain  others  are  inten- 
sified by  pressure,  and  that  this  is  dependent  upon  the  pitch  of  the  sound 
and  not  upon  the  site  of  its  production.  It  is  therefore  important  for  the 
observer  to  listen  carefully,  first  with  the  lightest  possible  pressure  upon 
the  stethoscope  and  then  with  gradually  increasing  pressure.  He  should 
do  this  consciously  and  as  a  matter  of  routine,  rather  than  allow  such 
sounds  to  escape  him  or  stumble  upon  them  by  accident. 

Moreover,  since  the  monaural  and  binaural  stethoscopes  each  intensify 
different  sounds,  both  should  be  used  in  any  important  or  dubious  case 
before  the  examination  is  concluded. 

Graphic  Methods. — As  stated  above,  the  most  accurate  and  reliable 
information  which  has  thus  far  been  obtained  is  that  obtained  by  means 
of  the  recording  microphone.     Unfortunately,  however,  all  the  methods 


102  DISEASES   OF   THE    HEART   AND    AORTA. 

thus  far  devised  have  been  too  cumbersome  for  the  bedside  or  even  for 
routine  hospital  use.  They  are  of  value  only  in  exceptional  cases  for  re- 
search, but  there  is  no  doubt  that  the  future  of  scientific  auscultation  lies 
in  this  field. 

"valvular  areas"  in  auscultation. 

The  various  cardiac  sounds  are  best  heard  over  certain  definite  locations 
corresponding  more  or  less  to  the  structures  in  which  they  arise,  but  par- 
ticularly to  the  course  of  the  blood  current  and  to  their  mode  of  origin 
(Fig.  100) .  Thus  the  sounds  produced  in  the  left  ventricle  are  best  heard 
at  the  apex;  those  produced  at  the  aortic  orifice,  though  produced  behind 
the  sternum,  are  heard  just  to  the  right  of  it  in  the  second  interspace;  the 
pulmonary  sounds  are  carried  to  the  second  left  interspace  at  the  sternal  mar- 
gin; while  the  sounds  from  the  right  ventricle  are  heard  over  the  entire  body 
of  the  sternum,  over  the  greater  part  of  the  area  of  absolute  dulness,  and  over 
the  base  of  the  ensiform  cartilage.     Abnormal  sounds,  murmurs,  etc.,  have, 

however,  a  different  distribution 
which  will  be  discussed  later. 

Normally  the  first  sound  at 
the  apex  and  everywhere  else 
below  the  third  rib  is  louder 
than  the  second  sound.  It  is 
also  of  longer  duration  than  the 
latter  (.08  second  as  compared 
to  .05).  Over  the  aortic  and 
pulmonic  areas  it  becomes  some- 
what fainter,  begins  a  trifle  later, 
and  is  of  longer  duration  than 
over  the  apex.  The  second  sound 
is  then  louder  than  the  first. 

Fig.  lOO.-The  "valvular  areas."  The    SeCOnd    SOUUd     at     the 

second  left  interspace  (pulmonic 
second)  is  usually  louder  than  that  over  the  second  right  (aortic  second)  up 
to  the  age  of  25  to  30,  when  the  latter  becomes  the  louder  (Cabot).'  This 
varies  greatly  in  different  individuals.  Mere  changes  in  blood-pressure  are 
not  sufficient  to  account  for  all  these  conditions,  since  the  pressure  in  the  pul- 
monary artery  is  never  more  than  half  that  in  the  aorta,  but  proximity  to 
the  sternum,  greater  elasticity  of  the  walls,  etc.,  combine  to  bring  about 
the  relative  loudness  of  the  second  pulmonic  sound,  and  therefore  any 
further  increase  in  pressure  in  either  artery  alters  the  relation  of  the  two 
sounds  to  each  other,  increased  pulmonary  pressure  increasing  the  pul- 
monic second,  increased  general  blood-pressure  increasing  the  second 
aortic,  etc.  The  progressive  thickening  of  the  aortic  semilunar  valves 
after  the  age  of  30  also  contributes  to  the  intensity  of  the  sound. 

Other  Sites  for  Auscultation. — Boy-Teissier  has  also  recommended  auscultation  in  the 
suprasternal  notch,  pressing  the  bell  of  the  stethoscope  as  far  down  behind  the 
manubrium  as  possible.     In  this  way  he  states  that  he  can  hear  aortic  diastolic  murmurs 

•  Directly  over  the  exposed  aorta  the  sound  is  louder  than  over  the  exposed  pulmo- 
nary artery.     (Thayer.) 


PHYSICAL   EXAMINATION. 


103 


Fi3.  101 . — The  propagation  of  the  heart  sounds  from  valves  to  chest  wall.  A.  Course  of  the  sound 
waves  within  the  heart.  B.  Propagation  of  the  heart  sounds  at  the  level  of  the  second  interspaces. 
C.  Propagation  of  the  sounds  at  the  level  of  the  fourth  and  fifth  interspaces. 


104  DISEASES   OF   THE   HEART   AND    AORTA. 

not  otherwise  audible.  He  thinks  that  he  is  also  better  able  to  distinguish  the  character  of 
aortic  systolic  murmurs.  The  method  has  never  gained  general  usage,  and  the  writer  is 
unable  to  find  in  it  any  of  the  advantages  claimed  by  Boy-Teissier.  The  chief  value  of 
suprasternal  auscultation  is  found  in  persons  whose  heart  sounds  are  feeble  or  inaudible 
over  the  precordium.  It  must  be  borne  in  mind,  however,  that  the  mitral  murmurs  are  not 
well  transmitted  to  this  region,  and  that  the  first  sound  heard  there  is  frequently  redupli- 
cated or  split. 

Another  form  of  auscultation  not  in  general  use  is  the  auscultation 
through  the  stomach- tube,  introduced  as  for  a  tracing  from  the  left  auricle. 
This  method,  first  used  by  A.  Hoffmann  in  1892,  has  been  revived  by  Gerhartz,  but,  though 
it  might  throw  some  light  upon  the  nature  of  an  occasional  mitral  murmur,  it  is  in  general 
difficult  and  very  inconvenient  to  carry  out;  and  in  many  cases  at  least  the  murmurs  are 
no  better  heard  than  over  the  chest  wall.  Nevertheless  where  it  is  important  to  know 
whether  a  murmur  is  conducted  back  into  the  left  auricle,  a  positive  finding  by  this  would 
be  conclusive. 

EMBRYOCARDIA. 

Ordinarily  the  diastolic  pause  between  sounds  is  longer  than  the  sys- 
tolic period,  and  the  interval  between  the  second  sound  of  one  cycle  and 
the  first  sound  of  the  next  is  longer  than  the  interval  between  the  first 
and  second  sounds  of  the  same  cycle.  However,  when  the  heart-rate  is 
very  rapid,  the  diastolic  pause  may  become  shortened  to  about  the  same 
interval  as  that  between  the  first  and  second  sounds  (long  pause  = 
short   pause),  so  that  the  sounds  succeed  one  another  at  uniform  inter- 


2  12  1 

Fig.  102. — Graphic  records  of  the  fetal  heart  sounds.     (After  Weiss  and  Joachim.) 

vals  like  the  ticking  of  a  clock.  This  rhythm  is  heard  normally  over  the 
fetal  heart  and  hence  has  been  termed  embryocardia  or  fetal  rhythm.  It 
also  occurs  in  adults  when  the  rate  is  very  rapid  (120  and  over),  and  hence 
under  conditions  in  which  the  heart  is  under  an  abnormal  strain  (see  page 
227),  as  in  fevers  with  high  temperature,  acute  heart  failure,  and  acute 
overwork  of  a  chronically  diseased  heart,  also  in  cases  of  paroxysmal  tachy- 
cardia and  allied  conditions.  Its  absolute  significance  is  simply  that  of  the 
rapid  heart -rate  to  which  it  corresponds. 

ACCESSORY   HEART   SOUNDS. 
REDUPLICATED    SOUNDS    AND    GALLOP    RHYTHMS. 

Reduplicated  Sounds. — Occasionally  one  or  the  other  of  the  two  normal 
heart  sounds  is  replaced  by  two  clear  sounds,  or,  in  other  words,  there  is  a 
reduplication.  This  reduplication  may  occupy  the  place  of  either  the  first 
or  the  second  sound,  and,  as  already  noted  by  Skoda,  it  may  seem  to  be 


PHYSICAL   EXAMINATION. 


105 


due  to,  (1)  splitting  of  the  normal  sounds  into  two  distinct  portions,  or 
(2)  pressure  of  an  accessory  sound  besides  the  normal  sound,  being  in  the 
latter  case  presystolic  (before  the  first  sound) ,  protodiastolic 
(shortly  after  the  second  sound) ,or  mesodiastolic  (in  mid-diastole) . 
The  relation  of  groups  1  and  2  to  one  another  and  to  the  cardiac  cycle  is 
shown  in  Fig-.  103. 


Intraventricular  Prkssure 


Volume  of  Ventricles 


Presystolic  Gallop 


Split  First  Sound 


Split  Second  Sound 


Protodiastolic  Gallop 


wn    m 


Z\ 


i: 


TE-LUB        DUB 


IIEE 


K-LUBDUB 


lO 


s 


LUB      DUB-L 


n 


T~ff 


LUB      DUB — DA 


13 


Fig.  103. — Diagram  illustrating  the  split  sounds  and  gallop  rhythms  and  their  phonetic  equivalents. 


As  to  the  causation  of  these  abnormal  sounds,  Uttle  definite  is  known.  A  great  deal 
of  the  indefiniteness  which  permeates  the  enormous  literature  upon  the  subject  is  due  to 
the  failure  of  the  writers  to  distinguish  clearly  between  the  different  forms  with  which 
they  are  dealing.  The  presystolic  and  protodiastolic  forms  are  grouped  under  one  head 
regardless  of  their  relations  to  mechanism  or  etiology;  it  is  mainly  due  to  the  writers  of  the 
French  school  under  the  leadership  of  Potain  that  the  differentiation  has  reached  even  its 
present  stage  of  development.  L.  Bard,  of  Geneva,  has  recently  given  an  excelleht  analysis 
of  the  subject  from  this  stand-point. 

According  to  Bard,  the  two  main  groups  of  accessory  sounds  are: 

(1)  The  presystoHc  gallop  reduplication  (tri-ta-tdt)  or  ta  tii  tat,  to  which  the  term 

1  3 

gallop  rhythm  should  be  limited,  most  commonly  met  in  nephritics  with  cardiac  hyper- 
trophy and  in  other  heavily  beating  hearts. 

(2)  The   protodiastolic   sound   ts'i  ta  ta  (lub-dub-da),  called   by  Bouillaud   bruit   de 

1  2 

rappel, — "sound  of  recall"  or  "diastolic  echo," — frequently  heard  at  the  apex  in  mitral 
stenosis.  Bard  thinks  that  the  above-mentioned  accessory  sounds  are  to  be  regarded  as 
merely  the  exaggeration  of  vibrations  normally  present  but  normally  inaudible. 

Split  Sounds. — The  sounds  (tlat-tat;  tat-tatl)  are  characterized  by  the 

12  12 

absolute  similarity  and  short  interval  between  the  two  portions,  and  may 
be  due  either  to  slight  asynchronism  of  the  two  ventricles  (C.  J.  B.  Williams, 
1836,  Skoda,  Gibson,  1874)  or  slight  separation  of  two  parts  of  the  ven- 
tricular sound,  which  are  of  different  origin  but  ordinarily  fused. 

As  has  been  seen,  the  ventricular  sound  contains  both  a  valvular  (auriculo ventric- 
ular) and  a  muscular  element,  and  perhaps  also  an  element  due  to  the  stretching  of  the 
walls  of  the  aorta.  Bard  thinks  that  variation  in  either  the  muscular  or  the  valvular 
element  might  give  rise  to  their  separation  into  two  sounds.  The  question  of  asynchronism 
of  the  two  ventricles  which  arises  in  this  connection  is  one  which  was  long  without  an 
experimental  basis,  but  the  recent  observations  of  Stassen,  Kraus  and  Nikolai,  and  Hew- 
lett indicate  the  possibility  that  it  may  occur  clinically.  Stassen,  in  Fredericq's  labora- 
tory, has  recorded  asynchronous  contractions  of  the  two  ventricles  when  the  latter  were 
recovering  from  vagus  inhibition,  and  also  with  ventricular  extrasystoles  produced  during 
periods  of  vagus  inhibition.  The  writer  has  on  one  occasion  heard  a  split  first  sound  in  an 
animal  in  which  the  contractions  of  both  ventricles  were  being  recorded  with  myocardio- 


106 


DISEASES   OF   THE   HEART   AND    AORTA. 


graphs.  The  ventricular  contractions  were  sHghtly  asynchronous.  In  a  number  of  other 
instances  in  which  no  spUt  first  sound  could  be  heard  the  contractions  were  absolutely 
synchronous.     However,  no  conclusions  are  justified  from  an  isolated  observation. 

The  splitting  of  the  first  sound  is  best  heard  over  the  base  and  body 
of  the  heart,  in  contrast  to  the  accessory  sounds  which  are  best  heard  at 
the  apex  (see  below).  As  to  the  splitting  of  the  second  sound,  this  likewise 
may  be  due  to  slight  asynchronism  of  the  two  ventricles,  or  to  the  fact  that 
even  without  this  the  semilunar  valves  may  not  close  at  exactly  the  same 
instant.  It  is  often  possible,  by  passing  the  stethoscope  along  the  second 
right  and  left  interspaces,  to  determine  which  second  sound  lags  behind. 

It  must  be  added,  however,  that,  as  Bard  himself  states,  no  accurate 
knowledge  of  either  the  split  sounds  or  the  accessory  sounds  can  be  gained 
until  they  are  registered  graphically  by  cardiophonographic  methods  along 
with  simultaneous  venous,  arterial,  or  cardiographic  tracings,  so  that  their 


APEX 


PHONOGRAM 


Ti,  SECONDS 


V^v/WW\/W\AAA/\A/VVVVV/VV¥V\AAA/VA/\/\/WVVAAAft/V\'VVV\A/VV\/^ 


PRE.     1     SYST. 


A  2  B 


Fig.  104. — Graphic  record  of  a  split  pulmonic  second  sound.  (After  Weiss  and  Joachim.)  PRE., 
presystolic  rumble;  SYST.,  systolic  murmur;  1,  first  heart  sound;  2  A,  B,  two  parts  of  split  second  sound 
(.04  sec.  apart). 

exact  relation  to  the  cardiac  cycle  may  be  determined.  So  rapid  is  the 
sequence  of  the  sounds  that  in  an  individual  case  the  differentiation  between 
spUt  and  accessory  sounds  is  often  difficult. 

Reduplication  of  the  First  Sound  from  Pericardial  Adhesions. — Reduplication  of  the 
first  sound  is  also  heard  in  a  number  of  cases  in  which  old  pericardial  and  pleural  adhesions 
are  found  at  autopsy  (Sewall),  which  may  be  easily  understood  to  give  an  abnormal  sound 
in  systole.  Just  how  commonly  this  group  occurs  has  not  been  determined  statistically, 
but  under  these  conditions  it  need  not  signify  any  disturbance  of  function. 

Presystolic  Gallop  Rhythm.  —  As  regards  the  accessory  sounds,  the 
great  majority  of  writers  take  the  view  suggested  by  Exchaquet  in  1875 
and  Johnson  in  1876  that  the  first  sound  of  gallop  rhythm  (presystolic 
sound)  is  due  to  the  vigorous  systole  of  the  auricle,  a  view  which  is  further 
supported  by  the  studies  of  Kriege  and  Schmall  (1891),  Friedrich  Miiller 
(1906),  G.  C.  Robinson  (1908),  and  others.  According  to  Miiller,  Marey 
believed  that  the  extra  sound  was  produced  by  the  auricle  sending  blood  into 
a  defectively  emptied  ventricle,  a  view  which  has  been  revived  by  Sewall. 
Moreover,  the  writer  has  been  able  to  show  on  the  excised  heart  that  when 
the  ventricles  are  distended  under  a  slight  positive  pressure  the  auriculo- 
ventricular  valves  may  open  along  only  a  small  extent  of  their  line  of  clos- 
ure. This  gives  rise  to  a  slight  functional  stenosis  at  the  point  where  they 
actually  open,  a  fact  which  may  account  for  the  audible  auricular  con- 
traction.    Miiller  considers  that  the  extra  tone  may  be  dependent  upon  a 


PHYSICAL   EXAMINATION. 


107 


delay  in  the  time  between  the  auricular  and  ventricular  contraction,  pos- 
sibly due  to  lowered  conductivity  in  the  atrioventricular  bundle  of  His, 
and  when  the  two  contractions  are  abnormally  separated  two  sounds 
instead  of  one  are  produced.  Tracings,  however,  do  not  usually  show 
delayed  conduction. 

All  these  writers  base  their  views  upon  the  fact  that  the  sound  appears  to  be  pre- 
systolic in  time  and  that  in  many  cases  a  well-marked  auricular  wave  may  be  seen  upon 
the  cardiogram  at  a  corresponding  point  of  the  cycle.  It  must  be  added  that  this  is  also 
seen  in  many  cases  in  which  there  is  no  gallop  rhythm,  and  that  it  seems  to  be  dependent 
more  upon  the  prominence  of  the  apex  impulse  in  the  interspace  facilitating  the  record 
than  it  does  upon  the  existence  of  the  sound.  However,  this  wave  is  often  quite  as  prom- 
inent in  the  curves  (protodiastohc  sound)  in  which  no  presystolic  sound  was  heard  as  in 
those  used  to  illustrate  the  gallop  rhythm  itself.  The  proof  is  therefore  insufficient,  but 
that  does  not  mean  that  the  theory  is  necessarily  wrong.  It  is  not  at  all  improbable  that 
the  forcible  contraction  of  an  overloading  auricle  may  give  an  audible  sound  just  as  it 
does  when  forcing  blood  through  a  narrowed  orifice  (presystolic  rumble),  but  this  has  not 
yet  been  proved  and  will  require  careful  investigation  with  the  cardiophonograph.  The 
possibility  of  functional  mitral  stenosis  like  those  mentioned  on  page  371  must  also  be  borne 
in  mind. 

Another  explanation  for  the  phenomenon  is  that  the  sound  occurs  during  the  ven- 
tricular systole,  as  suggested  by  H.  Chauveau,  who  thought  it  due  to  the  tension  of  the 
auriculoventriciilar  valves.  His  apex  tracings,  however,  are  not  carefully  timed  and  might 
quite  as  well  be  interpreted  as  evidence  of  the  auricular  sound. 

The  numerous  reviews  of  the  literature,  such  as  those  of  Obrastow,  Pawinski,  Robin- 
son, shed  no  further  light  upon  the  subject. 

Clinically,  the  presystolic  gallop  rhythm  is  usually  met  with  in  cases 
w4th  rapid  hypertrophied  hearts  which  are  under  a  slight  overstrain,  as  in 
the  classical  group  of  chronic  nephritis,  chronic  cardiac  disease,  aneurism, 
cases  with  arteriosclerosis,  exophthalmic  goitre,  mitral  stenosis,  and  acute 
fevers.  Occasionally  it  is  heard  in  normal  individuals  (Krehl) .  It  seems 
in  most  cases  to  accompany  slight 
overwork  of  the  heart,  but  its  me- 
chanical and  physiological  significance 
is  still  not  clear. 

Protodiastolic  Gallop  Rhythm. 
Third  Heart  Sound. — The  role  of  the 
protodiastolic  sound  (bruit  de  rappel, 
diastolic  echo)  seems  to  be  more 
definitely  established.  Though 
already  heard  by  Bouillaud  in  1835, 

in  mitral  stenosis,  its  occurrence  was  emphasized  by  Duroziez  (1874)  and  by 
Sansom  (1881),  who  term  it  the  "opening  snap"  of  the  mitral  valve,  indi- 
cating that  it  was  brought  about  by  the  opening  of  the  stiffened  valve. 
Barie  (1893)  and  Thayer  (1906)  called  attention  to  its  occurrence  in  normal 
individuals.  In  1907  the  writer  observed  this  sound  in  a  normal  individual 
with  a  slow  and  vigorous  heart,  whose  venous  pulse  showed  a  peculiar  extra 
wave  (Fig.  106,  h)  which  follows  the  inflow  of  blood  into  the  ventricle 
(as  indicated  by  the  normal  v  wave.  Fig.  106,  page  108) . 

The  writer  also  called  attention  to  the  fact  that  this  wave  bore  a  close  relation  to  the 
end  of  the  rapid  filling  of  the  heart  (or  diastole  proper)  upon  the  volume  curve  of  the  ven- 
tricles, and  that  Henderson  had  claimed  that  at  this  time  the  mitral  valves  and  triscupid 
were  closed  by  the  elastic  recoil  of  the  heart  walls.    That  this  actually  takes  place  and  is 


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Fig.  105.  —  Graphic   record   of   the  third  heart 
sound.    (Kindness  of  Prof.  Einthoven.) 


108 


DISEASES   OF  THE   HEART   AND   AORTA. 


dependent  upon  a  high  venous  pressure  can  be  shown  on  the  dead  heart  by  pouring  water 
into  the  ventricles  from  a  beaker  after  the  auricles  have  been  cut  off  in  the  manner  devised 


Fig.  106. — Jugular  and  carotid  tracings  from  a  iionnal  individual  witli  a  well-marked  third  heart 
sound,  showing  a  large  h  and  a  smaller  preauricular  wave  (w).  ?  indicates  a  small  wave  in  middiastole 
following  tlie  h  wave,  occasionally  found  though  perhaps  an  artefact. 


by  Baumgarten  (1843).  If  the  water  is  poured  from  just  above  the  valves  they  merely 
float  out  a  little  toward  the  middle  of  the  orifice;  if  from  the  height  of  about  10  cm.  they 
float  into  apposition;  if  from  50  cm.  above  they  are  left  tightly  closed  when  the  flow  ceases. 
These  observations  have  been  confirmed  recently  by  C.  Lian  in  Frangois-Franck's  labora- 
tory. Hirschfelder  also  suggested  that  this  clos- 
ure of  the  valves  may  be  sudden  and  vigorous 
enough  to  cause  a  sound.'  The  relation  of  this 
sound  to  this  portion  of  diastole  seemed  quite 
definite  by  comparison  with  a  graphic  record  of 
this  sound  made  at  about  the  same  date  by 
Einthoven  (Fig.  105),  which  shows  it  to  occur 
0.18  second  after  the  second  sound.  This  ex- 
planation has  also  been  supported  by  A.  G. 
Gibson  and  Professor  Thayer.  The  tracings  of 
Robinson,  who  was  investigating  the  subject 
from  a  different  stand-point,  have  also  shown 
the  constant  presence  of  the  h  wave  upon  the 
venous  tracings  accompanying  this  sound.  Rob- 
inson and  Thayer  have  also  shown  that  it  accom- 
panies a  wavelet  p  upon  the  cardiogram  in  early 
diastole  (Fig.  88,  I,  page  91),  probably  due  to 
the  filling  of  the  ventricles.  They  find  this  wave 
upon  the  cardiogram  in  almost  all  cases  of  pro- 
tocUastolic  gallop  rhythm,  and  regard  it  as  char- 
acteristic of  the  latter.  Thayer  has  demonstrated 
that  it  cannot  be  an  artefact,  since  it  is  often 
both  visible  and  palpable,  and  hence 
can  often  be  found  by  the  ordinary  simple 
methods  of  physical  examination.  Some  venous 
tracings  made  from  animals  by  Eyster,  along 
with  the  volume  curves  of  the  heart,  show  that 
the  rise  at  the  foot  of  the  h  wave  occurs  at  the 
According  to  these  explanations  the  sequence  of 
events  would  be  as  follows:  The  end  of  diastole  is  marked  by  the  second  heart  sound  and  by 
the  fall  in  the  cardiogram.  The  tricuspid  and  mitral  valves  open  almost  instantaneously,  but 
a  pf  riod  of  about  yV  second  is  required  before  the  fall  of  pressure  is  transmitted  to  the  jugu- 
lar vein  and  the  pressure  begins  to  fall  {v-y  collapse) .     The  inrush  of  blood  into  the  ventricles 


VOL 


Fig.  107. — Forces  supposetl  to  be  at  work 
in  the  production  of  the  third  heart  sound. 
Diastolic  closure  of  the  auriculoventricular 
valves.  Dotted  lines  indicate  the  direction 
of  inflow.  Black  arrows  indicate  the  recoil 
waves  tending  to  push  the  cusps  together. 

end  of  the  rapid  diastolic  filling  (Thayer). 


'  The  assumption  of  such  a  slapping  together  of  the  auriculoventricular  valves  at  the 
end  of  ventricular  filling  is  not  at  all  incompatible  with  the  fact  that  a  small  separation  ( 1-3 
mm.)  may  reappear  between  them  in  the  latter  part  of  diastole,  when  the  accumulation  of 
blood  in  the  auricles  has  become  sufficient  to  just  force  the  cusps  apart  (page  371). 


PHYSICAL   EXAMINATION.  109 

rapidly  distends  the  latter  until  they  reach  their  full  distention,  at  which  the  inflowceases  and 
the  cusps  of  both  mitral  and  tricuspid  valves  slap  together  (closing  slap  in  diastole). 
The  end  of  this  inflow  may  be  accompanied  by  a  slight  recoil  or  similar  movement  of  the 
ventricle,  giving  rise  to  the  small  wave  and  shock  noted  at  this  moment.  The  intensity 
of  this  recoil  is  probably  dependent  to  a  great  extent  upon  the  elasticity  (elastic  tissue) 
of  the  ventricular  walls;  hence  its  absence  in  old  persons.  Whether  the  feeble 
third  heart  sound  is  due  to  the  slapping  together  of  the  valves 
or  is  due  to  some  other  cause  cannot  be  stated  with  certainty.  After  the  period  of 
diastasis  (slower  inflow)  has  set  in,  the  blood  begins  to  accumulate  in  the  veins,  which 
are  distended  at  first  rapidly  and  later  in  diastole  more  gradually.'  The  angle  made  by 
these  two  portions  of  the  venous  curve  forms  the  h  wave.  The  foot  of  the  p  wave  com- 
mences at  the  end  of  the  period  of  rapid  ventricular  filling  and  corresponds  to  the  crest 
of  the  protodiastolic  wave  upon  the  cardiogram. 

A  'priori,  according  to  this  explanation  a  protodiastolic  sound  should 
be  heard  in  slow  hearts  because  in  them  the  ventricular  walls  are  distended 
to  their  full  extent  early  in  diastole;  in  cases  of  aortic  insufficiency  because 
of  the  high  intraventricular  pressure  which  tends  to  slap  the  cusps  of  the 
valves  together  early  in  diastole;  in  mitral  stenosis  owing  to  the  peculiar 
events  in  the  filling  of  the  ventricle  (vide  page  9),  and  perhaps  in  cases 
in  which  there  is  a  large  amount  of  residual  blood  in  the  ventricle  (dilata- 
tion) which  tends  to  diminish  and  shorten  the  period  of  inflow.  These 
represent  the  chief  conditions  in  which  it  is  actually  heard.  Thayer 
states  that  it  can  be  heard  at  the  apex  in  about  30  per 
cent,   of    normal   individuals   lying   upon   the   left    side. 

By  decades  its  frequency  was  as  follows;  First  decade  heard  in  58.9 
per  cent.;  second  decade  84.4  per  cent.;  third  decade  50.9  per  cent.;  fourth 
decade  42.3  per  cent.;  fifth  decade  14  per  cent.;  sixth  decade  and  after  0. 
It  seems  to  occur  in  practically  every  condition,  especially  in  cases  with 
slow  hearts,  and  seems  to  bear  no  definite  relation  to  cardiac  weakness. 

MURMURS. 

MECHANICAL   FACTORS    IN    THE    PRODUCTION    OF    MURMURS. 

As  has  been  seen  above  (page  92),  when  a  narrowing  occurs  in  the 
lumen  of  an  flastic-walled  tube  through  which  liquid  is  flowing,  eddies  are 
formed  which  set  the  walls  of  the  tube  into  vibration  and  give  rise  to  a  pal- 
pable thrill.  Accompanying  the  thrill  a  blowing  sound  known  as  a  "  mur- 
mur" may  be  heard  over  the  tube;  which,  like  the  thrill,  is  heard  much 
better  below  the  obstruction  than  above  it,  and  is  transmitted  in  the  direc- 
tion of  the  flow^  The  character  of  a  murmur  depends  upon  the  width  of 
the  orifice  at  which  it  is  produced,  upon  the  nature  of  the  walls  of  the 
orifice,  upon  the  velocity  and  tension  under  which  the  fluid  passes  through 
it,  and  upon  the  direction  in  which  the  flow  occurs. 

In  this  way  a  valvular  orifice  may  be  compared  to  the  larynx 
with  its  vocal  cords.  When  the  cords  are  lax  and  wide  apart,  the  air  moving  over  them  in 
even  forced  respiration  gives  no  sound;  when  the  cords  are  approximated  a  little  but  still 
held  loosely,  it  gives  a  whispered  "ch"  sound,  and  when  they  are  held  very  tense  true 
vocal  sound  is  heard.  Similarly,  no  sound  can  be  heard  over  the  excised  heart  when  the 
fluid  regurgitates  through  an  absolutely  patent  mitral  orifice  (Fig.  108) ;  if  one  of  the  chordae 
tendineaj  be  stretched  and  the  regurgitation  takes  place  through  a  small  slit  whose  walls 

*  It  is  not  improbable  that,  though  the  cusps  are  in  apposition  along  the  greater  part 
of  their  line  of  closure,  they  are  separated  at  a  few  points  during  diastasis. 


no 


DISEASES   OF   THE    HEART    AND    AORTA. 


are  flabby  (relative  insufficiency,  Fig.  108),  a  soft  low  blowing  murmur  will  be  heard  (the 
smaller  this  orifice  the  higher  pitched  and  more  distinct  the  murmur);  while  if  some  more 
or  less  hard  irregular  body,  like  calcified  vegetation,  is  situated  at  the  orifice,  this  acts  more 
or  less  as  a  resonator,  increases  the  sound,  and  may  even  give  it  a  roaring  or  a  squeaking 
(musical)  character.' 


Fig.  108. — Similarity  between  production  of  voice  sounds  and  the  production  of  murmuri?.  (Kindness 
of  the  J.  Am.  M.  Asso.)  A,  B,  C,  vocal  cords ;  D,  E,  F,  auriculoventricular  valves;  G,  H,  I,  aortic  and  pul- 
monic valves.  A  (high  note),  D,  G,  small  leaks  producing  high-pitched  murmurs;  B  (low  note),  E,  H, 
larger  leaks  producing  low-pitcned  murmurs ;  C,  F,  I,  very  large  leaks,  producing  no  murmurs. 

Occasionally  murmurs  become  so  loud  as  to  be  heard  several  feet  away 
from  the  chest  or  even  across  the  room.  Such  murmurs  are  usually  systolic 
in  time  and  are  often  due  to  calcified  vegetations,  arterial  plaques,  or  aortic 
or  mitral  stenosis.  As  in  the  larynx,  the  character  of  the  sound  produced 
at  a  valvular  orifice  is  due  not  only  to  the  size  and  shape  of  the  orifice,  but 
also  to  the  tenseness  of  the  walls  and  velocity  of  blood  flow  through  it,  and 
hence  is  largely  dependent  upon  the  height  of  the  blood-pressure.  All 
these  factors,  both  the  widening  of  the  leak  and  the  decreased  force  of  the 
beat,  explain  the  fact  that  as  the  heart  weakens  under  the  influence  of  the 
lesion  the  murmur  may  acutally  disappear. 


CHAR.\CTER    OF    MURMURS. 

Murmurs  may  be  roughly  divided  into  the  following  classes:  (1)  Direct  mur- 
murs best  transmitted  in  the  direction  of  the  blood  flow,  as  from  stenoses  or  calcified 
plaques;  (2)  Regurgitant  murmurs  due  tea  flow  in  the  direction  opposite  to  the 

'  Musical  or  squeaking  murmurs  are  sometimes  due  to  the  presence  of  tense  mod- 
erator bands  stretching  across  the  ventricular  cavity  and  resounding  like  banjo  strings, 
although  usually  these  bands  do  not  cause  murmurs  at  all. 

Very  frequently  they  arise  in  dilated  right  ventricles  in  association  with  functional 
tricuspid  and  perhaps  functional  pulmonary  insufficiencies.  They  are  usually  systohc, 
but  sometimes  diastolic  in  time.     They  are  often  cardiopulmonary. 


PHYSICAL   EXAMINATION.  Ill 

usual  blood  flow  (as  in  mitral  and  aortic  insufficiencies);  (3)  To-and-fro  "machinery" 
murmurs  which  occur  in  both  systole  and  diastole  in  congenital  heart  lesions;  (4)  Rum- 
bling murmurs. 

Of  these  1,  2,  and  3  are  more  or  less  blowing  or  roaring  in  character; 
while  the  rumbling  murmurs  are  devoid  of  this  character,  and  are  rumbling 
or  echoing,  more  like  a  series  of  heart  sounds  which  vary  in  intensity  (mitral 
stenosis,  Flint  murmur)  than  like  murmurs  due  to  the  passing  of  a  stream 
through  an  orifice. 

Brockbank  claims  that  these  may  be  produced  upon  a  model  by  means  of  a  stream 
flowing  through  a  conical  valve  from  apex  to  the  base  of  the  cone.  The  mechanism  of  the 
production  of  such  murmurs  is  still  very  obscure,  and  further  researches  are  necessary 
before  satisfactory  elucidation  can  be  given. 

"accidental,"    "h^MIC,  "    AND    "CARDIOPULMONARY"    MURMURS. 

Murmurs  over  the  heart  without  the  presence  of  valvular  lesions  are 
so  common  that  autopsy  evidence  led  Laennec  to  the  erroneous  belief  that 
murmurs  (bruits  de  soufflet)  were  of  no  diagnostic  importance  whatever. 

Such  murmurs  are  designated  by  various  terms :  "Haemic,"on 
the  assumption  that  they  are  always  due  to  anaemia,  hydrsemia,  or  other 
changes  in  the  quality  of  the  blood ;  "Functional"  or  "inorganic," 
because  they  are  not  associated  with  organic  lesion;  "Cardiopulmo- 
nary" or  "cardiorespiratory,"  on  the  assumption  that  they  arise  in  the 
lung  above  the  heart  and  not  in  the  heart  itself;  and  "Accidental,"  since 
they  are  not  associated  with  any  discernible  alteration  in  form  or  function. 
These  terms  are  not  mutually  exclusive;  but,  since  the  term  "functional" 
has  been  used  to  designate  conditions  in  which  there  is  actual  leakage 
owing  to  muscular  weakness,  and  since  "  inorganic  "  should  include  both 
"functional"  and  "accidental,"  the  term  ''accidental"  appears  to  be 
the  one  most  generally  useful.  Thus,  one  murmur  may  be  said  to  be  an 
accidental  murmur  of  ha^mic  origin,  while  in  another  case  the  accidental 
murmur  may  be  of  cardiopulmonary  origin. 

Occurrence  of  Accidental  Murmurs. — Potain,  who  has  made  the  most  extensive  inves- 
tigations upon  the  subject,  found  such  murmurs  in  one-eighth  of  all  the  patients  seen  in  his 
hospital  service.  It  was  present  in  almost  all  his  cases  of  Basedow's  disease  (exophthalmic 
goitre).  In  chlorosis  the  frequency  was  50  per  cent.;  in  rheumatism,  measles,  and  scarlet 
fever  20-25  per  cont.;  in  typhoid,  16  per  cent.;  in  pulmonary  affections,  5-10  per  cent. 
These  murmurs  were  common  in  subjects  in  the  first  three  decades  of  life,  reaching  maxi- 
mum frequency  at  the  ages  from  20  to  30,  and  gradually  decreased  in  frequency  after  the 
age  of  30.  For  description  of  the  murmurs  Potain  divided  the  precordium  into  the  fol- 
lowing regions:  1.  About  the  apex  (apical  zone);  2.  Above  the  apex  (supra-apical);  3. 
Lateral  from  the  apex  (para-apical) ;  4.  In  front  of  the  infundibulum  and  conus  arteriosus 
of  the  pulmonary  artery  (pre-infundibular);  5.  A  zone  between  the  pre -infundibular 
region  and  the  apex  (left  preventricular) ;  6.  An  area  behind  the  sternum  (sternal  region); 
7.  A  region  behind  the  xiphoid  (xiphoid  region).  The  murmurs  are  most  common  in  the 
region  lying  between  the  pulmonary  area  and  the  apex  (Potain's  left  ventricular  region), 
— that  is,  in  the  region  above  the  right  ventricle  and  the  interventricular  septum. 

Character  of  Accidental  Murmurs. — T  hese  murmurs  usually 
are  soft  and  blowing,  and  often  seem  rather  super- 
ficial. They  vary  greatly  when  the  patient  changes 
his   position.     Sometimes  they  are  best  heard  when  the  patient  is 


112  DISEASES   OF   THE   HEART    AND    AORTA. 

Ij-ing  down  and  diminish  or  disappear  entirely  when  he  stands  or  sits 
up;  sometimes  they  appear  only  when  the  patient's  position  is  vertical 
and  disappear  on  his  lying  down.  They  also  vary  with  the  phases  of 
respiration. 

Time  of  Accidental  Murmurs.  —  As  regards  their  occurrence  in  the 
cardiac  cycle,  accidental  murmurs  are  most  commonly  systolic  in  time, 
though  occasionally  diastolic.  Potain  calls  attention  to  the  fact  that  mur- 
murs may  occupy  either  the  whole  of  systole  (holosystolic)  or  only 
a  portion  of  it.  The  latter  may  occur  only  at  the  very  beginning  of  systole 
(protosystolic),  so  that  they  accompany  or  replace  the  first  heart 
sound.  Or,  they  may  be  heard  in  midsystole  (mesosystolic),  in 
which  case  they  follow  the  first  sound  but  are  separated  from  the  second 
sound  by  the  short  pause,  which  is  then  somewhat  shorter  than  usual. 
Or,  they  may  occur  at  the  very  end  of  systole  (tele  systolic)  and 
end,  without  interruption,  in  the  second  sound.  According  to  Potain, 
the  murmurs  of  mitral  and  tricuspid  insufficiency 
are  heard  throughout  the  entire  duration  of  systole, 
a  view  which  is  confirmed  by  the  graphic  records  of  Einthoven  and  Weiss 
and  Joachim.  The  accidental  murmurs,  however,  are  con- 
fined to  only  a  portion  of  systole.  Potain  believes 
that,  as  a  rule,  they  are  entirely  mesosystolic;  while 
Weiss  and  Joachim,  from  both  auscultatory  and  graphic  evidence  (Fig. 
110),  believe  that  they  also  accompany  and  modify  the  first  sound  though 
they  do  not  replace  it;  in  other  words,  that  they  occupy  both  the  proto- 
systolic and  the  mesosystolic  portions  of  the  systole. 

Sahli  states  that  accidental  murmurs  never  occupy  the  very  end  of 
systole  (telesystolic,  Potain;  prediastolic),  but  Potain  has  shown  that 
though  such  murmurs  are  rare  they  occur  occasionally. 

Accidental  diastolic  murmurs  are  also  rather  common,  and  may  occur 
either  in  the  aortic  region,  behind  the  sternum,  or  along  the  upper  left 
border  of  cardiac  dulness.  Occasionally  they  are  heard  at  the  apex.  They 
are  usually  short  superficial  puffs  following  a  well-marked  second  sound 
and  lasting  during  only  a  short  portion  of  early  diastole. 

Differential  Diagnosis  of  Accidental  Murmurs. — Potain  gives  the  following  points  in 
which  other  murmurs  differ  from  the  cardiopulmonary. 

1.  Pulmonary  Stenosis:  loud,  rough  holosystolic  murmur,  maximum  in 
second  left  interspace,  transmitted  toward  left  clavicle;  always  accompanied  by  a  thrill. 
The  accidental  murmur  is  soft,  often  mesosystolic,  devoid  of  thrill. 

2.  Pulmonary  Insufficiency:  diastolic  murmur  maximum  in  second  left 
interspace;  pulmonic  second  sound  absent  or  diminished.  The  accidental  diastolic  murmurs 
very  rarely  have  their  maximum  in  the  second  left  interspace. 

3.  Aortic  Stenosis:  rough  holosystolic  murmur,  maximum  in  second  right 
interspace,  propagated  toward  right  clavicle;  accompanied  by  thrill.  The  heart  is  hyper- 
trophied.  The  accidental  or  cardiopulmonary  murmur  in  this  region  is  more  superficial, 
soft,  and  changes  on  change  of  position. 

4.  Anaemia:  murmur  very  similar  to  that  of  aortic  stenosis,  but  the  thrill  is  less 
marked  and  the  heart  is  small  or  dilated  rather  than  hypertrophied. 

5.  Aortic  Insufficiency:  murmur  commences  exactly  at  the  beginning  of 
the  second  sound  and  almost  entirely  fills  diastole;  whereas  the  cardiopulmonary  diastolic 
murmur  follows  the  second  sound,  often  after  a  short  intervening  pause  {i.e.,  the  murmur  is 
mesodiastolic) .  Both  aortic  and  accidental  murmurs  are  of  wide  distribution,  embracing 
the  entire  precordium,  and  varying  greatly  with  change  of  position. 


PHYSICAL   EXAMINATION  113 

6.  Patent  Septum  of  the  Ventricles:  holosystolic  murmur  loudest  at 
the  third  left  interspace;  rough,  always  accompanied  by  a  thrill;  whereas  the  accidental 
and  cardiopulmonary  murmurs  are  not. 

7.  Mitral  Insufficiency:  murmur  holosystolic,  usually  rather  rough,  maxi- 
mum at  the  apex.  The  cardiopulmonary  murmur  may  have  its  maximum  two  or  three 
centimetres  lateral  wards  from  the  apex;  and  this  is  usually  associated  with  a  systolic  retrac- 
tion at  the  apex. 

8.  Tricuspid  Insufficiency:  murmur  maximum  over  sternum  and  xiphoid 
process.  There  is  an  increased  area  of  flatness  (hypertrophy  of  ventricles).  This  murmur 
is  also  increased  by  leaning  forwards  so  as  to  throw  the  heart  against  the  chest  wall. 

Nature  and  Causation  of  Accidental  Murmurs. — The  facts  mentioned 
above  apply  to  a  large  number  of  cases  in  which  murmurs  have  been  heard 
during  life,  but  in  which  no  leaks  and  no  lesions  of  the  heart  were  demon- 
strable at  autopsy. 

A  large  variety  of  factors  have  been  mentioned  to  explain  these  accidental  murmurs: 

Haemic  Murmurs. — Bouillaud  was  the  first  to  call  attention  to  the  fact  that  mur- 
murs were  more  readily  produced  in  the  less  viscous  blood  of 
anaemia  than  under  normal  conditions;  a  fact  which  was  subsequently 
verified  by  Cohnheim;  but  Bouillaud  himself  realized  that,  though  anaemia  might  give  rise  to 
some  of  the  accidental  murmurs,  there  were  many  cases  in  which  it  could  not  be  a  factor. 
The  blood  counts  made  in  later  decades  have  entirely  substantiated  Bouillaud's  conserva- 
tism. However,  numerous  observers  from  Bouillaud's  time  to  the  present  have  adhered 
to  the  "hsemic"  origin  of  the  accidental  murmurs.  Sahli  goes  so  far  as  to  state  that 
they  may  in  reality  be  only  venous  hums  transmitted  to  the 
ventricles,  though  he  does  not  explain  why  they  should  be  systolic  in  time.  Even 
though  this  explanation  is  inadequate,  it  is  certain  that  in  cases  of  grave  anaemia  such  trans- 
mitted murmurs  do  arise.  They  are  heard  very  loudly  over  the  aorta  and  second  right 
interspace,  but  are  loud,  rough,  and  superficial,  quite  different  from  the  gentle  blow  of  the 
usual  accidental  murmurs. 

Functional  Insufficiency  of  the  Auriculoventricular  Valves,  especially  of  the  mitral, 
was  supposed  by  Naunyn  to  be  the  chief  cause  of  the  accidental  murmur  in  the  pulmonary 
area.  Naunyn  believed  that  this  murmur  was  transmitted  from  the  left  auricle  directly  to 
the  pulmonary  artery  and  thence  to  the  chest  wall  in  the  pulmonary  area.  However,  in 
these  cases  the  murmur  may  not  be  heard  at  all  in  those  areas  in  which  the  definite  mitral 
and  tricuspid  murmurs  are  best  heard.  Functional  insufficiency  of  the  tricuspid  valve 
has  also  been  assumed,  but  this  is  rendered  improbable  by  the  fact  that  these  murmurs  have 
a  very  different  distribution  from  those  of  the  tricuspid  and  are  rarely  heard  over  the 
xiphoid  process.  In  dogs  the  writer  has  found  accidental  murmurs  very  common;  but, 
in  contrast  to  the  murmurs  in  tricuspid  or  mitral  insufficiency,  these  accidental 
murmurs  cannot  be  heard  over  the  right  or  left  auricle.  In  man 
also  they  are  not  heard  over  the  region  of  the  right  auricle,  even  when  the  patient  is  made 
to  lean  forward  and  the  walls  of  that  chamber  are  thus  pressed  against  the  chest  wall. 

Functional  Stenosis  of  the  Pulmonary  Artery  and  Infundibulum  has  been  assumed  by 
Luethje  in  order  to  explain  the  production  of  systolic  murmurs  in  the  pulmonary  area. 
It  is  true  that  the  pulmonary  artery  makes  a  sharp  bend  just  behind  the  second  left  inter- 
space; and  also,  as  Romberg  and  others  have  shown,  that  often  the  accidental  murmur  is 
increased  by  pressure  with  the  stethoscope.  Against  this  view  are  the  softness  of  the 
murmur,  the  absence  of  a  thrill,  and  the  fact  that  it  is  not  transmitted  toward  the  left 
shoulder,  but  is  well  heard  over  the  right  ventricle.  Moreover,  in  dogs  the  accidental  mur- 
mur may  persist  in  practically  every  position  in  which  the  heart  may  be  held. 

Eddy  Currents  within  the  Ventricles. — Hilton  Fagge  has  called  attention  to  the  fact 
that  eddy  currents  may  arise  within  the  ventricles,  as  the  blood  passes  between  the  papillary 
muscles  and  the  trabeculae  carneae :  that  these  may  strike  against  the  bases  of  the  papillary 
muscles  and  the  chordae  tendineae,  set  them  into  vibration  while  they  are  tense  during 
systole,  and  thus  give  rise  to  a  systolic  murmur.  Although  Fagge  himself  believed  that 
this  would  apply  only  to  a  dilated  heart,  it  seems  also  applicable  to  a  small  heart,  since 
during  systole  the  apertures  between  the  walls  and  the  papillary  muscles  are  smaller  and 
more  slit  like.  However,  the  explanation  lacks  confirmation. 
8 


114 


DISEASES   OF   THE   HEART    AND    AORTA. 


Similar  to  this  view  is  the  old-time  assumption  that  accidental  blowing  as  well  as 
musical  murmurs  indicated  the  presence  of  a  moderator  band  across  the  chamber  of  the 
right  ventricle,  but  this  is  not  borne  out  by  autopsy  experience. 

Cardiopulmonary  Factors. — Laennec  in  1826  wrote:  "In  certain  persons  the  pleurse 
and  the  anterior  borders  of  the  lungs  extend  in  front  of  the  heart  and  cover  it  almost  entirely. 
If  one  examines  such  a  person  when  his  heart  is  beating  more  forci- 
bly than  usual,  the  diastole  of  the  heart,  compressing  these 
portions  of  the  lungs  and  forcing  the  air  out  of  them,  alters  the 
breath  sounds  in  such  a  way  that  it  imitates  a  blowing  murmur  or  the  sound  of  wood  file. 
But  with  a  little  skill  it  becomes  easy  to  distinguish  this  sound  from  a  cardiac  murmur. 
It  is  more  superficial;  one  hears  the  normal  heart  sounds  be- 
low it;  and  it  disappears  almost  entirely  when  the  patient  is 
made   to   hold   his   breath   for  a   few  moments.''' 

Physiological  experiments  have  borne  out  Laennec's  claim  that  the  lung  moves  to  and 
fro  with  each  cardiac  cycle  (Buisson,  Voit,  van  der  Heul,  Landois,  Meltzer).  but  have  demon- 
strated that  the  most  sudden  movement  of  the  air  accompanies  the  rarefaction  of  the  air 

within  the  lung  during  systole,  rather 
than  its  extrusion  during  diastole. 

The  cardiopulmonary  murmurs 
formed  the  subject  of  an  exhaustive 
study  from  1865  to  1894  by  Potain, 
many  of  whose  data  have  been  given 
above.  Potain  controlled  the  findings 
by  auscultation  with  carefully  made 
cardiograms  and  experimental  studies 
and  found  that: 

1 .  The  cardiopulmonary  murmurs 
are  loudest  and  most  frequent  in 
those  regions  (infundibulum  and  vicin- 
ity of  the  pulmonary  artery')  where 
the  movement  of  the  heart  is  greatest. 

2.  They  occur  in  regions 
and  in  phases  of  the  car- 
diac cycle  at  which  the  car- 
diogram shows  retractions 
of  the  interspace  (areas  of 
negative  pressure  with  sudden  expan- 
sion of  the  lung). 

Hence,  the  systolic  murmur  is  most  common  over  the  infundibulum  and  right  ven- 
tricle, over  which  there  is  usually  a  systolic  retraction  (see  page  91  and  Fig.  89). 

If  the  retraction  (fall  in  the  cardiogram)  occurs  in  the  middle  of  systole,  the  murmur 
is  found  to  be  mesosystolic;  if  at  the  end  of  systole,  the  murmur  is  telesystolic ;  if  the  fall  is 
in  diastole,  the  murmur  is  diastolic.  Indeed  Potain  encountered  several  cases  in  which 
the  form  of  the  cardiogram  changed  upon  alteration  of  the  position  of  the  patient;  and 
corresponding  to  the  period  of  greatest  retraction  the  murmur  over  the  area  changed  from 
mesosystolic  to  diastolic. 

This  is  a  surprising  confirmation  of  the  theory  of  cardiopulmonary  murmurs.  There 
can  indeed  be  no  doubt  that  cardiopulmonary  murmurs  are  frequent,  and  that  they  form 
a  very  considerable  proportion  of  "accidental"  murmurs.  Besides  the  blowing  murmurs 
referred  to  above,  it  is  probable  that  many  of  the  so-called  "musical"  or  "squeak- 
ing" murmurs  are  of  cardiopulmonary  origin,  and  are  really  piping  rales  produced  by  the 

*  "  Chez  quelques  sujets,  les  plevres  et  les  bords  anterieurs  des  poumons  se  prolongent 
au-devant  du  cceur  et  le  recouvrent  presque  entierement.  Si  Ton  explore  un  pareil  sujet 
au  moment  ou  il  ^prouve  des  battements  du  cceur  un  peu  ^nergiques,  la  diastole  du  coeur 
comprimant  ces  portions  du  poumon  et  en  exprimant  Fair,  altere  le  bruit  de  la  respiration 
de  maniere  a  ce  qu'il  imite  plus  ou  moins  bien  celui  d'un  soufflet  donne  par  le  cceur  lui- 
meme:  il  est  plus  superficiel;  on  entend  au  dessous  le  bruit  naturel  du  coeur;  et  en  recom- 
mandant  au  malade  de  retenir  pendant  quelques  instants  sa  respiration,  il  diminue  beau- 
coup  ou  cesse  presque  entierement." 


Fig.  109. — Distribution  of  the  accidental  murmur. 


PHYSICAL   EXAMINATION.  115 

to-and-fro  movement  in  the  lung  during  either  phase  of  the  cardiac  cycle.  Other  rales  of 
cardiopulmonary  origin  more  closely  resembling  the  sonorous  and  crepitant  rales 
of  respiration  are  also  very  common  along  the  margin  of  the  left  lung.  Moreover,  the  breath 
sounds  themselves  are  frequently  modified  by  the  cardiac  movements,  giving  rise  to  the  so- 
called  cog-wheel  type  of  breathing;  in  which  inspiration  is  interrupted  by  a  series 
of  small  clicks  and  pauses  coincident  with  and  due  to  the  effects  of  cardiac  contractions 
upon  the  air  in  the  lungs.  The  cog-wheel  type  of  breathing  is  often  associated  with  slight 
changes  in  the  overlying  lung  and  is  thus  often  a  premonitory  sign  of  pulmonary  tuberculosis. 

Differentiation  between  Cardiopulmonary  and  other  Accidental  Mur= 
murs. — However,  in  spite  of  the  frequency  of  cardiopulmonary  murmurs, 
it  is  probable  that  Potain  erred  in  ascribing  all  accidental  or  non-valvular 
murmurs  to  this  origin.  In  the  first  place,  many  such  murmurs  are  audible 
over  the  area  of  cardiac  flatness  several  centimetres  from  the  lung  borders, 
when  breath  sounds  which  are  of  equal  loudness  over  the  lung  cannot  be 


CAROTID 


PHONOGRAM 


Fig.  110. — Graphic  record  of  an  accidental  murmur.     (After  Weiss  and  Joachim.) 

heard  at  all  at  these  sites.  Secondly,  the  murmurs  can  be  well  heard  directly 
over  the  exposed  dogs'  hearts  when  the  lung  has  been  entirely  retracted, 
and  when  valvular  insufficiencies  and  stenoses  can  be  absolutely  excluded. 
For  the  present,  therefore,  it  must  be  admitted  that  there  are  still 
many  uncertainties  in  the  differentiation  between  cardiopulmonary  and 
other  accidental  murmurs.  The  diagnosis  of  the  former  must 
be  confined  to  murmurs  of  distinctly  superficial 
quality  which  are  heard  loudest  over  the  lung  bor- 
ders and  are  absent  or  much  diminished  over  the  area 
of  cardiac  flatness,  and  w-hich  vary  with  change  of  position. 
The  diagnosis  may  be  considered  as  rendered  probable  if  the  area  over 
which  the  murmur  is  heard  moves  tow'ard  the  sternum  in  inspiration  and 
away  from  it  in  expiration,  corresponding  to  the  movement  of  the  marginal 
strip  of  lung.  If  the  reverse  is  the  case  and  the  area  of  intensity  extends 
lateralward  in  expiration  and  recedes  toward  the  sternum  in  inspiration, 
the  murmur  is  more  likely  to  arise  within  the  heart. 

Imitations  of  the  Heart  Sounds. — A  remarkably  accurate  method  for  imitating  the 
heart  sounds,  reduplications,  and  rough  or  blowing  murmurs  has  been  used  for  the  past 
three  years  by  the  writer's  colleague.  Dr.  Charles  W.  Larned.  This  is  carried  out  by  placing 
the  palm  of  the  observer's  hand  tightly  over  his  ear,  and  then  tapping  upon  the  elbow 
with  the  finger  tips  of  the  other  hand.  The  blow  must  be  struck  with  loose  finger-joints. 
Its  force  can  be  varied  to  suit  variations  in  the  loudness  of  the  sound.  Dull  and 
distant  sounds  may  be  imitated  by  light  blows  of  the  finger  or  by  raising  the  palm  of  the 
hand  from  the  ear,  snapping  sounds  by  pressing  the  hand  tightly  upon  the  ear  and 
executing  a  sharp  stroke.     Blowing  murmurs  are  reproduced  by  a  gentle  stroking  of  the 


116 


DISEASES   OF   THE    HEART    AND    AORTA. 


elbow.  Dr.  Henry  Lee  Smith  has  modified  this  procedure  by  striking  the  blows  directly 
upon  the  back  of  the  hand,  instead  of  the  elbow,  a  method  by  which  sharper  and  more 
snapping  sounds  can  be  produced.  He  is  able  to  give  a  very  accurate  reproduction  of  the 
presystolic  rumble  and  snapping  first  sound  of  mitral  stenosis  by  bringing  all  the  four  fingers 
down  upon  the  knuckles  or  metacarpals  in  as  rapid  succession  as  possible,  a  manoeuvre 
which  is  best  executed  by  a  quick  pronation  from  the  elbow.  The  blow  struck  with  the 
index  finger  (snapping  first  sound)  should  be  somewhat  louder  than  the  rest. 

While  these  methods  are  excellent  for  demonstrating  to  one  student  at  a  time,  they 
cannot  be  used  for  demonstrating  to  a  whole  group  simultaneously.  For  this  purpose  the 
writer  has  resorted  to  the  somewhat  cruder  method  of  executing  the  same  taps  and  strokes 
upon  the  top  of  a  derby  or  even  a  soft  felt  hat.  This  imitation  is  not  quite  so  accurate, 
and  the  snapping  and  rumbling  quality  are  not  reproduced,  but  nevertheless  it  enables 
the  instructor  to  point  out  the  salient  features  to  all  and  to  illustrate  their  main  variations 
and  relations  to  the  events  of  the  cardiac  cycle. 


INTRAVENTRICULAR 
PRESSURE 


VOLUME   OF 
VENTRICLES 


MITRAL  SYSTOLIC 
AORTIC  SYSTOLIC 
AORTIC  DIASTOLIC 
PRESYSTOLIC 


Fig.  111. — Diagram  showing  the  relation  of  the  more  common  simple  murmurs  to  events  of  the 
cardiac  cycle.  Solid  black  bars  indicate  the  heart  sounds.  Vertical  parallel  lines  reaching  to  the  base 
indicate  blowing  or  rough  murmur.    Wavy  vertical  lines  not  reaching  to  the  base  indicate  a  rumble. 

The  exact  method  for  the  reproduction  of  each  sound  or  murmur  can  thus  be  indi- 
cated schematically  by  designating  the  finger  to  be  used  (I  =  index,  M  =  middle,  R  =  ring 
finger,  L  =  little  finger)  and  the  accent  of  the  sound'.  Time  intervals  may  be  shown  by 
dashes,  and  rapid  succession  of  the  split  sounds  by  bracketing  the  corresponding  letters. 
Murmurs  are  indicated  by  stroke. 

Thus:  r — I  =  Normal  first  sound  at  the  apex;  I — I' =  Normal  first  sound  at  aorta; 
stroke  I' =  Mitral  murmur;  I — (I'M)=Split  second  sound;  (IM — I)=Split  first  sound; 
(I-M' — I)  =  Presystolic  gallop;  I — I'-M  =  Protodiastolic  gallop;  I  stroke  I  =  Mesosystolic 
murmur;  LRMI' — I  =  Presystolic  murmur;  I — stroke  =  Diastolic  blowing  murmur  replac- 
ing second  sound;  I — I  stroke  =  Diastonc  murmur  following  the  second  sound;  LRMI' 
stroke  I  =  PresystoHc  systolic  murmur  of  mitral  stenosis;  Gentle  to-and-fro  rubbing  of 
skin  =  Pericardial  friction. 

Relations  of  the  Simple  Murmurs  to  Events  of  the  Cardiac  Cycle. — The  relations  of 
the  simple  cardiac  murmurs  to  the  contractions  of  the  cardiac  chambers,  as  well  as  to  the 
filling  and  emptying  of  the  ventricles,  is  shown  in  Fig.  111.  The  mechanism  of  their 
production  will  be  discussed  in  detail  in  connection  with  the  valvular  lesions  to  which 
they  correspond.  It  will  be  seen,  however,  that  the  mitral  systolic  murmur  begins 
coincidently  with  the  first  heart  sound  before  the  blood  flows  into  the  aorta,  and  that 
it  continues  throughout  systole;  that  the  aortic  systolic  murmur  follows  the  first  sound 
and  is  loudest  in  midsystole;  that  the  aortic  diastolic  murmur  is  loudest  in  early  diastole, 
when  the  filling  of  the  heart  and  the  regurgitation  are  most  rapid;  and  that  the  presys- 
tolic rumble  is  produced  by  the  inrush  of  blood  into  the  ventricles  during  auricular  systole. 


PHYSICAL   EXAMINATION. 


117 


SINGLE  MURMURS. 


Time. 


Character. 


Phonetic ' 
equivalents. 


Distribution. 


Clinical  condition. 


Presystolic  . 


Systolic . 


Mesosystolic  or  tel- 
esystolic  (predi- 
astolic) 


Diastolic. 


Mid-diastolic, 


Rumbling,  occasion- 
ally blowing 


Blowing  or  roaring. 
Enters  into  or  re- 
places as  well  as 
follows  first  sound. 
Uniform  or  decres- 
cendo 

Blowing  or  roaring; 
follows  first  sound; 
has  a  crescendo 
character  in  mid- 
systole  and  decres 
cendo  in  late  sys- 
tole 

Similar  in  character 
to  aortic  systolic 
murmur 


Soft  blowing,  uni- 
form or  decres- 
cendo 


Blowing  . 


Rumble 


ftat-ta;   trat-at;   tr- 
r-rub-dub 


shush-dub;  jjje-dub; 
ssh-dub;     faf-tam 


luzsch-dub;   taf-dub 


lujsch-dub;  taf-dub; 

1  2 

taf-tam 


lupff-dub;      taf-tat; 

1  2 

luff-dub 


lupd-shsh; 
lup-dush; 


tam-taf; 
lup-shsh 


lub-dub-tra. 


Apex  only,  lower 
precordium  be- 
tween parasternal 
line  and  sternum 

Over  bo<ly  of  heart, 
at  apex  and  to  ax- 
illa, often  at  back. 
Over  lower  ster- 
num and  neighbor- 
ing precordium 

Loudest  over  2d 
right  interspace ; 
thrill  also  in  ves- 
sels of  neck.  Not 
so  loud  at  apex 


2d  left  interspace 
and  to  left  of  ster- 
num (thrill) .  Else- 
where over  chest 
(thrill) 

Over  entire  precord- 
ium, esp.  2d  and 
3d  left  interspace. 
Varying  with 
change  of  position. 
Not  transmitted 
beyond  apex 

.\t  2d  rib  near  ster- 
nal margin;  loud- 
est over  sternum 
at  level  of  2d  left 
interspace  and  in 
the  latter  near  the 
sternal  margin 

At  2d  left  inter- 
space and  right 
sternal  margin  ; 
also  to  right  of 
sternum 

At  2d  left  interspace 
and  sternal  margin 


At  apex  only. 


Mitral     stenosis ;    tri- 
cuspid atenosis. 


Mitral  insufficiency; 
tricuspid  insuffi- 
ciency. 


Sclerosis  of  aorta; 
aortic  stenosis;  con- 
genital heart  lesion. 


Pulmonary  stenosis, 
congenital  heart  le- 
sion, aneurism. 


Functional,  accident- 
al, or  anaemic  mur- 
mur. Ansemic  fever; 
neurasthenia  etc.  - 
sometimes  organ- 
ic (?). 


Aortic  insufficiency. 


Pulmonary 
ency. 


insuffici- 


With  no  other  marked 
signs  of  valvular  in- 
sufficiency. Abnor- 
mal murmur  (Potain, 
Graham,  Steele). 

Mitral  stenosis;  some 
cases  with  pericard- 
ial adhesions,  etc. 


1  These  phonetic  equivalents  most  closely  imitate  the  cardiac  sounds  when  the  consonants  are 
prolonged  as  much  as  possible. 


COMBINED  MURMURS. 


Time. 


Presystolic  (Flint 
murmur),  systol- 
ic, and  diastolic 


Character. 


Presystolic  rumble; 
systolic  blow;  di- 
astolic blow 


Phonetic 
equivalents. 


ftaftash;       tr-r-rub- 

2 

dush 


Distribution . 


Blow  loudest  at  2d 
right  and  2d  left  in- 
terspaces; at  apex 
and  out  in  axilla. 
Rumble  over  apex 
only 


Clinical  condition. 


Vegetation  at  aortic 
valve,  aortic  insuf- 
ficiency. Sometimes, 
but  not  necessarily, 
mitral  insufficiency, 
occasionally  also 
mitral    stenosis. 


118 


DISEASES   OF   THE    HEART    AND    AORTA. 


COMBINED  MURMURS  (Continued). 


Time. 


Character. 


Phonetic 
equivalents. 


Distribution. 


Clinical  condition. 


Systolic    and    di-   Systolic    and    dias-   taf-tash;   lush-dush;    2d  right  and  left  in-   Aortic       insufficiency 


a^tolic 


Same 


tolic  blow 


Same. 


shush-shush 


Same. 


terspace,  .sternum, 
left  sternal  mar- 
gin. transmitte<l  to 
arteries 


with  aortitis;    aortic 
stenosis. 


Loudest  at  left  ster-  Pulmonary      stenosis 

nal   margin;    thrill  and        insufficiency; 

maximuni   to   first  open  ductus  arterio- 

and      .second      left  sus;     other  congeni- 

interspace  tal  heart  lesions. 


Irregularly  in  both   Soft,   superficial,    slush-dush;   slush-  Over  the  entire  pre-   Fibrinous  pericarditis. 


systole    and    di-      scratchy 
astole  I 


Accompanies  both    Pleuropericardial 
heart  sounds  and 
both   breath 
sounds 


Crepitant;  small  ex- 
plosive  r&les 


Pleuropericarditis. 


cordium.  especial- 
ly over  the  area  of 
absolute  dulness;| 
increased  by  pres- 
sure with  stetho- 
scope I 
i 
Over  relative  cardi- 
ac dulness  onlj" 
.scratch  simultane- 
ous with  respira- 
tion as  well  as 
cardiac  cycle.  In- 
creased by  pres- 
sure with  stetho- 
scope 


Over  relative  cardi-|  Emphysema.      Inter- 


ac  dulness  only 


stitial  emphysema. 


VASCULAR    SOUNDS    AND    MURMURS. 

Arterial. — Besides  the  murmurs  transmitted  from  the  heart,  murmurs 
also  occasionally  arise  in  the  arteries  themselves.  A  systolic  murmur  and 
an  audible  first  sound  (pistol-shot  tone)  may  be  produced  by  pressure  with 
the  stethoscope  over  the  arteries,  but  without  exerting  a  definite  pressure 
it  may  often  be  found  accompanying  the  dilatation  of  markedly  pulsating 
arteries,  as  in  aortic  insufficiency  and  with  dicrotic  pulses,  etc.  The  eddies 
arising  in  an  aneurism  usually  give  rise  to  a  rough  or  blowing  systolic 
murmur  which  may  be  transmitted  for  a  considerable  distance  along  the 
arteries.  In  aortic  insufficiency  a  double  murmur  (sytolic  and  diastolic) 
may  be  heard  over  the  arteries  (Duroziez). 

Venous. — A  sound  is  heard  over  the  jugular  vein,  especially  over  the 
jugular  bulb  just  above  the  clavicle,  in  cases  of  marked  anaemia,  chlorosis, 
etc.  (Camac).  The  murmur  is  humming  or  roaring  in  character  and 
occurs  during  both  systole  and  diastole  (humming-top  murmur,  "bruit 
du  diable,"  etc.).  Weiss  and  Joachim  have  registered  the  sound  and  have 
shown  that  it  never  ceases.  As  shown  by  Cohnheim  the  anaemic  blood 
flows  more  rapidly  than  does  normal  blood,  probably  owing  to  its  lower 
viscosity;  and  both  these  factors  facilitate  the  production  of  a  murmur. 
However,  it  has  not  yet  been  shown  that  the  murmur  is  loudest  at 
those  periods  of  the  cardiac  cycle  during  which  the  flow  in  the  veins  is 
most  rapid. 


PHYSICAL   EXAMIXATIOX.  119 


MURMURS    AS    AN    AID    TO    DIAGNOSIS. 

It  is  evident  from  what  has  gone  before,  as  well  as  from  the  consensus 
of  medical  practice,  that  auscultation  furnishes  a  most  important  means 
of  diagnosis  of  cardiac  lesions.  It  is  equally  evident  that  each  abnormal 
sound  may  be  associated  with  any  one  of  several  clinical  conditions,  which 
must  be  still  further  differentiated  from  one  another,  not  only  by  the  mur- 
mur but  by  its  distribution,  transmission,  and  variations,  but  particularly 
by  the  other  methods  of  physical  examination,  graphic  methods,  and 
X-ray  examination.  The  examiner  should  not  content  himself  with  a 
simple  designation  of  the  lesion,  but  should  become  fully  conversant 
with  the  disturbance  of  function  in  all  parts  of  the  circulatory  system, 
and  with  its  remote  secondary  effects. 

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Bard,  L.:  Du  bruit  de  galop  de  I'hypertrophie  du  ccEur  gauche,  Sem.  m^d.,  Paris,  1906, 
xxvi,  229.     Also  De  la  multiplicity  anormale  des  bruits  du  coeur,  ibid.,  1908,  xxviii,  3. 

Kriege  and  Schmall:  Ueber  den  Galopprhj^hmus  des  Herzens,  Ztschr.  f.  klin.  Med.,  Berlin, 
1891,  xviii. 

Miiller,  F.:  Ueber  Galopprhythmus  des  Herzens,  Mvinchen  med.  Wchnschr.,  1906,  liii,  785. 

Marey,  E.  J.:  La  Circulation  du  sang  k  l'4tat  physiologique  et  dans  les  maladies,  Par.,  1881. 

Sewall,  H.:  On  a  Common  Form  of  Reduplication  of  the  First  Sound  of  the  Heart,  Contrib. 
Sci.  Med.  (Vaughan),  Ann  Arbor,  1903,  29;  also,  A  Common  Modification  of  the  First 
Sound  of  the  Normal  Heart  Simulating  that  heard  with  Mitral  Stenosis,  Am.  J.  M. 
Sc,  1909,  cxxxviii. 

Robinson,  G.  C:  Gallop  Rhythm  of  the  Heart,  Am.  J.  M.  Sci.,  Phila.,  1908,  cxxxv,  670. 

Chauveau,  H.:  Etude  cardiographique  sur  la  m^canisme  du  bruit  de  galop.  Thesis,  Paris, 
1902. 

Pawinski,  J.:  Die  Entstehung  und  khnische  Bedeutung  des  Galopprhythmus  des  Herzens, 
Ztschr.  f.  kUn.  Med.,  Berl.,  1907,  Ixiv,  70. 

Duroziez  and  Sansom:  Quoted  from  Bard. 

Hirschfelder,  A.  D.:  Some  Variations  in  the  Form  of  the  Venous  Pulse,  Bull.  Johns  Hop- 
kins Hosp.,  1907,  xviii,  265. 

Einthoven,  W.:  Ein  dritter  Herzton,  Arch.  f.  d.  ges.  Physiol.,  Bonn,  1907,  cxx,  31. 

Gibson,  A.  G.:  Upon  a  Hitherto  Undescribed  Wave  in  the  Venous  Pulse,  Lancet,  Lend., 
1907,  ii,  1380. 

Thayer,  W.  S.:  On  the  Early  Diastolic  Heart  Sound  (the  So-called  Third  Heart  Sound), 
Bost.  M.  and  S.  J.,  1908,  clviii,  713;  Further  Observations  on  the  Third  Heart  Sound, 
Arch.  Int.  Med.,  Chicago,  1909,  iv,  297. 

Potain:  La  Clinique  m^dicale  de  la  Charity,  Par.,  1894. 

Laeimec,  Bouillaud,  Hilton  Fagge:  quoted  from  Potain. 

Luethje:  quoted  from  Brugsch  and  Schittenhelm,  Lehrbuch  Klinischer  Untersuchungs- 
methoden, Berl.,  1908. 

Buisson,  Voit,  van  der  Heul,  quoted  from  Meltzer,  S.  J.:  On  the  Nature  of  Cardio-pneu- 
matic  Movements,  Am.  J.  Physiol.,  Bost.,  1899,  i,  117.  Also,  Sanders,  G.:  Cardiopul- 
monary Murmurs,  Edinb.  M.  J.,  1897,  N.  S.,  i,  522. 

Stengel,  A.:  The  Significance  of  Systolic  Murmurs  over  the  Apex  and  Base  of  the  Heart, 
Cleveland  J.  M.,  1898,  iii,  191;  and  Foshay,  P.  M.:  A  Case  of  Cardiopulmonary  Mur- 
mur Illustrating  the  Importance  of  Differentiation,  ibid.,  1901,  vi,  236. 

Putnam,  J.  J.:  The  Clinical  Associations  and  Significance  of  the  Cardiopulmonary  Murmur, 
Tr.  Ass.  Am.  Phys.,  Phila.,  1903,  xviii,  157. 


PART  II. 

I. 

PRIMARY  CARDIAC  OVERSTRAIN. 

It  has  long  been  known  that  heart  failure  may  arise  from  simple  over- 
strain of  the  heart  without  the  intervention  of  any  actual  cardiac  symptoms. 
This  condition  usually  remains  acute  and  ends  in  rapid  recovery,  but  it 
may  also  become  chronic  and  reduce  the  patient  to  lasting  invalidism.  In 
its  worst  form  such  a  purely  functional  weakening  of  the  heart  may  result 
in  death. 

This  conception  was  first  introduced  by  Stokes  in  1854,  and  was  con- 
firmed later  by  studies  of  Clifford  Allbutt,  A.  R.  B.  Myers,  and  Peacock  in 
England,  and  da  Costa  in  America.  Their  articles  were  collected,  trans- 
lated into  German,  and  published,  along  with  an  excellent  monograph 
upon  the  subject,  by  Johannes  Seitz,  of  Zurich,  in  1875,  bringing  them  to 
the  cognizance  of  the  German  writers.  In  1886  v.  Leyden  added  important 
contributions.  In  1898  the  matter  was  subjected  to  clinical  experiment 
by  Theodor  Schott,  whose  conclusions  have  been  disputed  by  a  host  of 
later  and  more  careful  observers. 

The  most  interesting,  extensive,  and  complete  of  all  these  papers  are 
those  of  da  Costa,  based  upon  several  hundred  cases  occurring  among 
Union  soldiers  of  the  Civil  War.  It  is  impossible  to  do  justice  to  these 
studies  in  a  brief  abstract.  His  presentation  is  so  complete  and  so  nearly 
a  model  of  clinical  study  for  its  time  that  the  reader  is  urged  to  consult 
the  original  publication. 

CLINICAL   CASES. 

A  very  typical  case  of  da  Costa's  series  is  illustrated  by  the  following 
history. 

Case  I. — Irritable  heart,  chiefly  from  hard  service;  recovery. 
— Wm.  Henry  H.,  private  68th  Pennsylvania  Vol.,  admitted  into  the  Turner's  Lane  Hospital 
in  Philadelphia,  November  2,  1863,  having  just  returned  from  a  furlough.  He  enlisted  in 
August,  1862,  at  the  time  in  good  health,  though  he  had  suffered  occasionally  from  rheu- 
matism. He  did  a  great  deal  of  hard  duty  with  his  regiment.  Some  time  before  the  battle 
of  Fredericksburg,  he  had  an  attack  of  diarrhoea;  after  the  battle,  he  was  seized  with 
lancinating  pains  in  the  cardiac  region,  so  intense  that  he  was 
obliged  to  throw  himself  down  upon  the  ground,  with  palpitation. 
These  symptoms  frequently  returned  while  on  the  march,  were  attended  with  dimness  of 
vision  and  giddiness,  and  obliged  him  often  to  fall  out  from  his  company  and  ride  in  the 
ambulance.  Yet  he  remained  with  his  regiment  until  J  u  1  y  4,  1863,  when  he  was  wounded 
at  the  battle  of  Gettysburg.  The  wound  healed  in  about  one  month;  but  the  cardiac 
symptoms  became  worse,  and  violent  palpitations  ensued  upon  the  slightest  exertion, 
sometimes  also  whilst  in  bed,  obliging  him  to  rise.     There  was  soreness  in  the  cardiac 

121 


122  DISEASES   OF   THE   HEART   AND    AORTA. 

region,  and  a  constant  dull  pain.  The  impulse  was  extended,  slightly  jerky,  96,  and  of 
irregular  rhythm,  some  beats  following  one  another  in  rapid  succession;  the  first  sound  was 
feeble,  the  second  very  distinct.  The  man  did  not  look  sick.  Height  5  feet  7  inches; 
measured  31  inches  around  the  chest  one  inch  below  the  nipple;  he  did  not  smoke;  chewed 
tobacco  in  moderation. 

The  patient  did  not  improve  under  aconite;  but  under  digitalis  the  impulse  became 
quiet  and  78,  and  on  March  23,  having  previously  done  duty  as  orderly,  he  was  detailed 
on  police  duty,  and  his  treatment  stopped.  The  heart  continuing  to  act  regularly, 
he  returned  to  his  regiment  May  3,  1864. 

Another  case,  quoted  from  v.  Leyden,  illustrates  the  various  phases 
of  the  malady  very  well. 

Case  II. — Carl  Timm,  butcher,  aged  30.  Family  history  negative.  Syphilis  ten  years 
before,  quiescent  for  several  years.  Otherwise  always  healthy.  Performed  military  service 
for  5  years  without  any  trouble.  In  the  fall  of  1880  became  a  butcher  in  the  Charite  Hospital 
where  he  had  to  lift  and  chop  sides  of  beef  weighing  200  lbs.  The 
first  symptoms  appeared  suddenly  on  the  afternoon  of  December  30,  1880,  during  an 
ordinary  day's  work,  when  he  felt  a  severe  pressure  in  the  pit  of  the  stomach, 
preventing  him  from  taking  a  deep  breath  and  causing  him  to  stop  in  his  work.  At  this 
time  he  noticed  palpitation  and  irregularity  of  the  heart.  For  several  days 
after  this  he  did  no  heavy  work  and  then  felt  well.  When  he  tried  to  do  heavy 
lifting  again  the  same  pain  and  sensation  of  pressure  returned,  and 
though  he  continued  his  work  he  was  compelled  to  stop  for  breath  from  time  to  time.  On 
Feb.  17,  1881,  the  pain  became  very  intense  and  he  entered  the  hospital  on  Feb.  21. 

Physical  Examination. — Patient  is  a  very  well-built  young  man,  well  muscled,  well 
nourished  but  not  fat.  Complexion  florid  but  healthy  looking.  No  dyspnoea  or 
cyanosis.  Moderate  oedema  of  lower  extremities.  Patient  complains  only 
of  palpitation  of  the  heart.  The  pulse  is  strikingly  irregular  so  that  it  is  im- 
possible to  count.  The  radial  arteries  are  small,  blood-pressure  apparently  low.  The 
cardiac  impulse  is  intense,  vibratory,  and  very  irregular.  Apex  impulse  is  in 
5  th  left  interspace  2  cm.  beyond  mammillary  1  i  n  e  ,  well  marked,  read- 
ily palpable.  Cardiac  dulness  begins  above  at  3d  rib,  extending  below  to  6th  rib,  and 
reaching  just  to  the  right  of  the  sternum.  Heart  sounds  are  feeble  and  unequal  but 
clear.  Lungs  clear.  Liver  and  spleen  are  not  enlarged.  Urine  500  c.c,  sp.  gr.  1023,  no 
albumin. 

Ordered  rest  in  bed,  ice-bag  over  heart,  infusion  of  digitalis  every 
2  hours.  Within  a  few  days  symptoms  and  cedema  had  subsided,  but  the 
irregular  heart  action  persisted.  By  March  20  he  was  well  enough  to  be  discharged,  with 
the  following  note:  Apex  beat  0.5  cm.  to  left  of  mammillary  lino;  first  sound  at  apex 
loud  and  ringing,  second  sound  distant  but  clear;  pulse  irregular;  examination  otherwise 
negative. 

This  represents  the  first  stage  of  his  illness,  in  which  the  following 
features  are  noteworthy:  1.  A  very  strong  and  perfectly  healthy  young 
man  suffers  from  heart  failure  as  the  immediate  result  of  overstrain.  The 
first  attack  came  on  suddenly  while  at  work  and  passed  off  soon,  but  attacks 
recurred  whenever  the  patient  did  heavy  work,  and  he  was  compelled  to 
enter  the  hospital.  2.  Physical  findings:  heart  dilated  especially  in  the 
longitudinal  axis,  weak  apex  beat  (dilatation  of  left  ventricle),  great  cardiac 
irregularity.  3.  Relatively  rapid  improvement  after  rest  in  bed  and  digi- 
talis. 4.  The  heart  then  returned  to  almost  normal  size,  but  the  irregu- 
larity in  rhythm  persisted. 

Second  Stage. — Patient  returned  to  his  old  work  in  spite  of  warning, 
and  within  two  months  oedema  of  the  legs  had  again  set  in  and  he  was  confined  to 
bed  for  eight  weeks  more.  Returning  to  work  again,  he  could  perform  only 
very  light  labor,  and  very  soon  returned  once  more  to  the  hospital  for  seven  weeks, 
with  still  more  marked  oedema.    Once  more  these  disturbances  disappeared  after  rest  and 


PRIMARY  CARDIAC   OVERSTRAIN.  123 

digitalis,  but  thereafter  the  sUghtest  work  caused  palpitation  and  the  feeling  as  though 
there  were  a  tight  c  o  rd  about  the  chest.  He  also  felt  pain  in  the  region  of  the 
liver.  At  this  point  he  re-entered  the  hospital.  Pulse  180,  small,  irregular.  Face  flushed, 
no  cyanosis.  Expression  depressed.  Skin  normal;  oedema  of  feet  and  legs.  Gangrene  of 
big  toe  of  right  foot.  Respiration  a  little  rapid,  dyspnoea  only  on  exercise,  but  while  walk- 
ing he  often  stops  to  catch  his  breath.  Occasionally  he  has  attacks  of  dyspnoea  lasting 
about  10  minutes,  beginning  with  a  feehrg  of  pressure  in  the  region  of  the  heart.  He 
then  feels  as  though  hot  liquid  were  pouring  from  the  heart  upwards  to  each  side  of 
the  neck. 

Physical  Signs. — A  pex  beat  in  6th  left  interspace  in  anterior  axillary 
line,  soft  and  easily  compressed.  Heart  therefore  much  enlarged,  sounds  clear  and  fairly 
loud,  action  markedly  irregular.     Liver  enlarged  and  tender. 

Ordered  rest  in  bed,  digitalis,  morphine  at  night.  Patient  became  much  better 
within  twenty-four  hours,  pulse  then  68  per  minute.  The  attacks  of  dyspnoea  almost 
disappeared.  Urine  1300,  sp.  gr.  1020.  Within  six  days  all  cardiac  symptoms  had  dis- 
appeared. March  11:  Pulse  52.  Feels  well,  no  pain.  Apex  beat  in  5th  left  interspace 
3  cm.  beyond  mammillary  line,  moderately  forceful.  Heart  sounds  clear  but  irregular. 
He  still  occasionally  has  feeling  of  pressure  in  chest. 

Features  of  second  stage:  1.  Dilatation  of  heart  much 
more  marked  than  before.  2.  Very  rapid  and  very  irregular 
heart  action.  3.  Definite  attacks  of  pain  in  heart  and  feeling  of  pressure 
(anginoid  in  character),  with  radiating  pains  in  shoulder  and  arm.  4.  Swell- 
ing of  liver  (failure  of  right  heart).  5.  Return  to  almost  normal  under 
treatment,  diminution  in  size  of  left  ventricle.  6.  Intercurrent  affections: 
small  infarct  of  lung,  pressure  gangrene  of  great  toe,  recovered  from. 

Third  Stage. — Returned  to  the  hospital  in  July,  1885  (two  years  later).  He  has  been 
able  to  do  very  little  since  last  admission.  Now  much  emaciated,  face  thin,  ap- 
pears depressed.  Cheeks  and  lips  slightly  cyanotic.  Respiration  dyspnoeic  and 
stertorous.    No  orthopnoea.     Moderate  oedema  of  shins. 

Cardiac  impulse  seen  in  5th  to  7th  left  interspaces,  apex  beat  felt  in  7th  in  axillary 
line,  forcible.  Heart  rate  about  132,  irregular.  Cardiac  dulness  19  cm.  from  left  sternal 
margin.  (Upper  limit  of  cardiac  dulness  as  before  begins  at  3d  rib.)  Liver  readily  pal- 
pable. Sounds  loud,  more  or  less  short  but  no  murmur.  Did  not  remain  in  hospital,  but 
on  October  4,  1885,  was  brought  in  again  in  collapse.  Marked  cyanosis,  extremities  cold, 
oedema  of  legs  up  to  knees.  Heart  as  before,  sounds  still  clear.  Pulse  150.  Liver  a  hand's 
breadth  below  costal  margin.  Ordered  digitalis,  also  camphor  subcutaneously,  tea  with 
cognac.  At  midnight  collapse  more  marked,  very  marked  dyspnoea  and  cyanosis;  threw 
himself  to  and  fro,  groaned  loudly.  Pulse  not  palpable,  not  revived  by  camphor  or  ether 
injection.  At  2  a.m.  became  quiet;  stertorous  breathing  set  in  at  3  a.m.;  died  quietly  at 
3.15  a.  m. 

Autopsy. — Marked  oedema  of  legs.  Both  lungs  slightly  retracted,  slightly  adherent 
over  apices.  Pericardium  distended,  little  fluid.  Heart  markedly  enlarged  (more 
than  twice  the  size  of  patient's  fist),  especially  in  the  longitudinal  axis.  Left  ventri- 
cle more  dilated  than  right.  Distance  from  insertion  of  pulmonary  arterj' 
to  apex  13  cm.,  to  right  border  of  heart  10  cm.  Length  of  left  ventricle  15  cm.  Little 
epicardial  fat.  Valves  normal,  aortic  valves  close  perfectly.  Papillary  muscles  well  devel- 
oped, some  trabeculae  flattened  and  undergoing  fibrous  changes.  A  fibrous  patch  is  seen 
on  the  interior  surface  of  the  left  ventricle.  Endocardium  otherwise  delicate,  showing 
some  yellow  areas  of  fatty  degeneration  of  the  endocardium  and  papillary  muscles.  Cut 
surface  of  heart  muscle  shows  cloudy  swelling.  Left  auricle  markedly  di- 
lated. Right  ventricle  appears  pale  with  spots  of  yellow.  Lungs,  oedema  of  bases. 
Liver,  markedly  enlarged;  definite  nutmeg  liver.  Kidneys,  large,  dark  red,  harder 
than  normal. 

Microscopic  examination  shows  extensive  fatty  degeneration  of  muscle-fibres,  but 
only  in  the  inner  layers.  No  interstitial  changes,  no  changes  in  blood-vessels 
or  nerves  of  the  heart.  Here  and  there  the  interstitial  strands  of  connective  tissue 
appeared  thicker  than  normal  but  without  cellular  infiltration. 


124  DISEASES   OF   THE   HEART   AND    AORTA. 


ETIOLOGY. 

In  da  Costa's  200  soldiers,  well-marked  fever  preceded  the  overstrain 
in  17  per  cent.;  diarrhoea  (among  which  there  may  have  been  many  mild 
cases  of  typhoid  fever)  30.5  per  cent.;  hard  field  service,  particularly  exces- 
sive marching,  38.5  per  cent.;  wounds,  injuries,  rheumatism,  scurvy,  ordi- 
nary duties  of  soldier  life,  and  doubtful  cases  18  per  cent.  Contrary  to  the 
belief  of  many  observers,  tobacco  did  not  seem  to  be  an  etiological  factor 
in  his  series. 

Allbutt  gives  the  following  etiological  factors  of  cardiac  overstrain: 
gymnastics,  rowing,  Alpine  climbing,  long-distance  running,  intense  fits 
of  anger  or  emotion,  sexual  excesses.  Overstrain  is  very  frequent  among 
miners,  metal  workers,  carriers  of  heavy  burdens,  blacksmiths,  moulders. 
Morton  Prince  calls  attention  to  the  development  of  cardiac  dilatation 
under  severe  mental  strain,  as  in  a  civil  service  examination.  Anaemia  and 
chlorosis  (Henschen),  apparently  mild  illnesses,  intestinal  disturbances, 
acute  alcoholism,  and  febrile  diseases  (Dietlen)  are  also  frequent  causes. 
Sexual  excess  is  an  important  factor,  especially  in  men;  but  its  effects 
are  usually  more  marked  in  hearts  already  weakened  from  other  diseases 
or  from  valvular  lesions  than  in  perfectly  healthy  hearts. 

Myers,  Allbutt,  and  Schott  have  shown  that  tight  belts,  uniforms, 
and  corsets  displace  the  heart  upward,  embarrass  its  action,  and  predispose 
to  overstrain.  Indeed  Myers  found  that  cavalry  soldiers  with  tight  belts 
suffered  more  from  long  rides  than  infantry  from  marching  the  same  dis- 
tance. 

SYMPTOMS,    SIGNS,    AND    CLINICAL    COURSE. 

The  chief  symptoms  are  dulness,  excitability,  nervousness,  loss  of 
sleep,  loss  of  appetite,  restlessness,  buzzing  in  the  ears,  vertigo,  muscae 
volitantes,  palpitation  of  the  heart,  usually  very  severe  and  often  asso- 
ciated with  a  feeling  of  pressure  or  constriction  over  the  chest.  This  may 
be  very  distressing,  but  does  not,  as  a  rule,  cause  the  patient  to  remain 
absolutely  still  nor  give  him  the  fear  of  sudden  death,  though  da  Costa 
mentions  cases  in  which  the  precordial  distress  was  great  enough  to  cause 
soldiers  to  fall  to  the  ground  in  the  midst  of  battle. 

Pain  over  the  precordium  and  the  left  shoulder,  occasionally  down 
the  arm,  increased  on  inspiration  and  on  coughing. 

Dull  headache,  dizziness,  especially  on  bending  over,  sleep- 
lessness, indigestion,  tympanites,  and  diarrhoea  are  common. 

The  patient  often  wears  an  anxious  expression  and  there  are  usually 
pallor  and  more  or  less  cyanosis.  Pulse  is  usually  small,  feeble,  rapid,  and 
often  irregular.  The  cardiac  impulse  may  be  barely  or  not  at  all  visible, 
but  on  percussion  the  area  of  relative  cardiac  dulness  is  usually  found  to  be 
enlarged  considerably  to  the  left  both  downward  and  upward,  and  often  also 
to  the  right  as  well.  This  corresponds  to  the  dilatation  of  the  left  ventricle 
and  of  both  auricles  (i.e.,  diameters  MR  and  ML,  Fig.  84,  are  much  increased) . 

On  the  other  hand  Katzenstein  has  shown  that  in  just  these  cases  the  impulse 
may  be  exceptionally  strong  and  impart  a  heaving  to  the  whole 
chest,  even  though  the  heart  be  much  dilated,  failing,  and  devoid 
of  the  slightest  trace  of  hypertrophy.    A  systolic  retraction  is  usually  seen  over  the  greater 


PRIMARY  CARDIAC   OVERSTRAIN. 


125 


part  of  the  precordium  of  these  overworking  hearts  (Fig.  89),  corresponding  to  the  con- 
traction of  the  right  ventricle  (page  91).  Occasionally  in  rapid  and  irregular  hearts  this 
appearance  is  somewhat  puzzling  and  has  led  some  clinicians  to  dictate  notes  of  "delirium 
cordis"  where  this  condition  was  not  present  at  all.' 

The  area  of  relative  cardiac  dulness  is  much  enlarged  (Fig. 
112),  especially  to  the  left,  both  downwards,  corresponding  to  the  dilata- 
tion of  the  ventricle,  and  upwards,  corresponding  to  the  auricle.  In  more 
severe  cases,  especially  with  marked  cyanosis,  the  dulness  is  enlarged 
also  to  the  right  from  dilatation  of  the  right  auricle.  Occasionally  this 
dilatation  may  have  passed  off  before  the  patient  has  been  seen  by  the 
physician  and  only  the  other 
symptoms  and  signs  persist,  but 
it  is  safe  to  assume  that  it  has 
been  present  at  an  earlier  stage 
of  the  disease. 

The  heart  sounds  may 
be  either  very  distant  and  feeble 
or  very  short  and  sharp,  corre- 
sponding to  the  two  types  of 
cardiac  impulse.  They  are  usu- 
ally unaccompanied  by  mur- 
murs, but  in  an  irregular  heart 
may  be  of  uneven  intensity. 
The  second  pulmonic  is  usually 
the  loudest  sound  heard.  The 
clearness  of  the  first  sound  is 
often  altered  by  a  reduplication, 
especially  in  rapid  hearts,  or  by 

the  presence  of  a  soft  blowing  systolic  murmur,  which  is  usually  loudest 
over  the  pulmonic  or  tricuspid  area,  but  occasionally  also  heard  to  the 
anterior  axilla.  These  sounds  do  not  always  but  may  sometimes  corre- 
spond to  the  presence  of  functional  insufficiency  of  the  mitral  valve 
(vide  page  323),  in  other  cases  to  anaemia.  It  is,  however,  extremely 
difficult  or  sometimes  impossible  to  decide  absolutely  whether  such  an 
insufficiency  is  present. 

The  pulse  is  usually  rapid,  ranging  from  80  to  160  per  minute, 
small,  and  weak,  in  many  cases  irregular  in  both  force  and  rhythm.  In 
less  severe  cases  there  are  only  occasional  extrasystoles  (Schott) ;  in  the 
more  advanced  there  is  an  absolutely  irregular  rhythm  which  persists 
even  after  the  rate  slows.  There  is  often  persistent  tachycardia  without 
dyspnoea,  lasting  for  even  weeks  or  months. 

Clinical  Course. — In  some  cases,  however,  all  the  signs  and  symptoms 
of  overstrain  may  be  present  without  any  irregularity  whatever,  but  often 
associated  with  a  rapid  and  regular  pulse.  Occasionally  the  pulse  may  be 
regular  only  while  it  is  rapid,  but  becomes  irregular  as  the  rate  diminishes. 
In  many  cases  no  murmurs  or  other  signs  of  valvular  insufficiency  are 

'  The  term  delirium  cordis  is  used  rather  indefinitely  to  designate  conditions 
varying  between  extreme  irregularity  with  tachycardia  and  true  fibrillation  of  the  heart. 
The  onset  of  the  latter  is,  however,  not  consistent  with  the  existence  of  life. 


Fig.  112. — Cardiac  dulness  in  \.  l.e,\dtir>  case  upon  his 
three  successive  admissions    (1,  II,  III). 


126    .  DISEASES   OF   THE   HEART   AND    AORTA. 

encountered,  while  in  still  others  a  relative  or  functional  insufficiency  of 
the  mitral  or  tricuspid  valve  results  from  the  cardiac  dilatation,  with  some 
embarrassment  of  the  heart  resulting  therefrom  in  addition  to  the  original 
failure.  Systolic  (functional)  murmurs  are  heard  in  these  areas,  and  the 
stasis  is  still  further  increased  by  the  regurgitation  of  blood.  The  oedema 
becomes  extreme,  hydrothorax  may  set  in,  and  death  soon  results.  As  in 
the  case  of  da  Costa's  patient  under  discussion,  the  progress  may  be  stayed 
somewhat  by  occasional  treatment  and  rest.  If  the  latter  is  sufficient  and 
the  disease  not  too  far  advanced,  the  patient's  life  may  be  saved. 

The  liver,  as  in  Case  II,  enlarges  when  the  condition  becomes  severe 
and  tricuspid  insufficiency  has  set  in.  Its  edge  is  then  smooth  and  varies 
in  consistency  from  being  rounded  and  so  soft  as  to  be  palpable  only 
with  the  side  of  the  index  finger  to  almost  board-like  hardness.  It  is 
always  smooth.  In  severe  cases  jaundice  may  be  present  and  the  liver  may 
pulsate. 

The  abdomen  is  often  distended  with  gas,  a  factor  which  contrib- 
utes largely  to  the  cardiac  discomfort  by  pushing  up  the  diaphragm.  In 
the  later  stages  of  heart  failure  ascites  may  be  present. 

The   genitalia  show  oedema  only  in  the  later  stages  of  the  disea.se. 

The  lower  extremities  are  often  oedematous,  the  swelling  first  mani- 
festing itself  about  ankles  and  shins. 

The  urine  during  the  period  of  heart  failure  is  usually  scant, — less 
than  900  c.c.  (30  ounces)  for  24  hours, — owing  to  diminished  rapidity  of  blood 
flow.  It  is  then  of  high  specific  gravity  (1020  and  over),  and  often  contains 
albumin  and  casts.  In  extreme  stasis  numerous  epithelial,  coarsely  and 
finely  granular,  and  hyaline  casts  are  seen  in  every  field  of  the  microscope. 

Blood.  The  blood  picture  may  vary  from  a  moderate  ana?mia  to 
a  real  polycythemia,  dependent  upon  the  condition  of  the  patient  before 
the  over-exertion. 

The  sputum  may  be  scanty  and  mucous,  or  profuse,  frothy,  and 
albuminous,  dependent  upon  the  relative  strength  of  the  right  and  left 
ventricles.  In  rare  cases  haemoptysis  results  during  the  exertion  from 
engorgement  of  the  pulmonary  capillaries. 

Transitory  Cardiac  Dilatation.  —  A  particularly  instructive  series  of 
cases  studied  with  modern  methods  are  those  reported  by  Hornung  (1908). 
Among  1100  cases  which  he  watched  with  the  X-ray  during  the  past  seven 
years  he  has  met  with  a  number  who  usually  showed  perfectly  normal 
hearts  but  were  subject  to  acute  dilatation  after  overstrain.  This  was 
particularly  frequent  in  persons  who  had  used  alcohol  to  excess,  in  those 
who  had  recently  suffered  from  infectious  diseases,  and  in  ansemic  indi- 
viduals. The  attacks  of  dilatation  are  brought  on  by  f  r i g h t , 
high  altitudes,  excitement,  over-exertion,  etc.  Sexual  ex- 
citement might  be  added  to  this  list.  Hornung  returns  to  the  old  view  of 
Seitz,  AUbutt,  and  v.  Leyden,  that  cardiac  overstrain  with  acute 
dilatation  is  much  more  common  than  might  be  supposed 
from  the  work  of  Moritz  and  his  pupils. 

For  a  long  period,  however,  he  may  be  expected  to  be  more  subject 
to  other  attacks  than  before,  although  by  care  he  may  remain  free  from 
them.     Just  how  long  this  susceptibility  may  last  varies  with  each  case, 


PRIMARY  CARDIAC   OVERSTRAIN.  127 

but  da  Costa  has  shown  us  that  after  carefully  sparing  the  patient  from  all 
severe  effort  for  weeks  or  even  months,  he  may  again  perform  even  such 
severe  efforts  as  are  entailed  on  cavalry  charges  and  forced  marches  without 
injury  and  may  lead  a  life  of  perfect  health. 

The  other  side  of  the  picture  is  shown  by  v.  Leyden's  case.  This  man 
returned  to  work  in  spite  of  the  discomfort.  The  latter  became  worse,  and 
after  bearing  it  for  three  months  he  entered  the  hospital  with  a  heart  already 
dilated  and  permanently  irregular,  and  with  well-marked  oedema  of  the 
limbs.  Definite  heart  failure  had  set  in.  From  this  he  recovered  under 
rest  and  treatment  with  digitalis.  His  heart  resumed  almost  normal  size, 
his  oedema  disappeared.  The  circulation  once  more  returned  to  almost 
normal,  but  one  permanent  injury  had  been  done  for  which  the  treatment 
was  of  no  avail.    The  heart  action  had  become  irregular  and  remained  so. 

The  commencement  of  permanent  absolute  irregularity  in  rate  (pulsus 
irregularis  perpetuus)  (see  Part  I,  Chapter  IV)  at  this  stage  is  a  very  com- 
mon occurrence  in  overstrained  hearts,  and  seems  to  be  one  of  the  most 
important  factors  in  determining  the  subsequent  course  of  the  disease  (see 
page  123).  When  the  irregularity  persists  it  adds  its  own  mechanical  effects 
on  the  circulation  to  those  already  present  and  increases  the  overstrain. 

When  a  life  of  strenuous  muscular  work  is  continued  by  such  a  patient 
the  result  is  inevitable.  Strain  follows  strain,  and  the  condition  brought 
about  by  the  first  failure  is  exaggerated  with  each  successive  day's  work. 
The  attacks  of  pain  and  pressure  in  the  thorax  (anginoid  attacks)  increase 
in  severity  and  frequency.  The  heart  dilates  more  and  becomes  corre- 
spondingly weaker.  Blood  stagnates  in  the  veins,  first  in  the  more  depend- 
ent portions,  causing  oedema  of  the  ankles,  shins,  thighs,  genitalia,  then 
enlargement  of  the  liver  and  ascites  from  stasis  in  the  portal  system,  finally 
oedema  of  the  face  and  arms.  The  heart  dilates  still  more;  the  mitral  and 
tricuspid  orifices  no  longer  close.  After  each  attack  he  is  less  vigorous 
than  before,  and  greater  care  must  be  taken  to  avoid  exertion.  For  the 
manual  laborer  such  a  life  may  be  at  once  impossible  and  intolerable,  but 
the  litterateur,  the  scholar,  the  scientist,  and  the  man  of  affairs  may  be 
saved  for  years  to  a  life  of  quiet  but  none  the  less  useful  activity  in  spite  of 
a  considerable  degree  of  cardiac  break-down. 

DIAGNOSIS. 

The  diagnosis  of  primary  overstrain  of  the  heart  is  not  always  simple. 
It  is  always  a  question  not  of  whether  the  heart  has  been  overstrained  but 
of  whether  this  weakening  is  primary,  and  whether  the  heart  was  perfectly 
healthy  before  the  effort  was  made.  If  the  heart,  muscle,  or  valves  were 
in  any  way  diseased  before  the  effort,  the  overstrain  may  be  considered  as 
secondary  to  that  lesion.  Accordingly  the  diagnosis  rests  upon  the  pre- 
vious histor}^,  upon  the  nature,  duration,  and  sequelae  of  previous  infec- 
tious diseases,  upon  the  degree  of  arteriosclerosis,  and  upon  the  general 
health  of  the  patient  before  the  onset  of  the  trouble. 

Latent  myocarditis,  fatty  degeneration,  and  arteriosclerosis  are  par- 
ticularly difficult  to  exclude.  A  mild  grade  of  myocarditis  may  have  given 
no  symptom  whatever  in  daily  life,  but  become  apparent  when  exercise 
is  violent.    A  mild  grade  of  arteriosclerosis  is  practically  universal  among 


128  DISEASES   OF   THE   HEART   AND   AORTA. 

persons  past  middle  age,  but  if  considerable  efforts  had  been  made  without 
symptoms  of  cardiac  insufficiency  these  may  be  disregarded.  When  symp- 
toms of  heart  failure  occur  suddenly  in  a  robust  individual  during  or  after 
some  intense  muscular  or  nervous  effort,  acute  cardiac  dilatation  and  over- 
strain may  usually  be  diagnosed  with  certainty,  but,  like  hysteria  among 
the  nervous  diseases,  it  should  be  arrived  at  only  after  a  process  of  careful 
exclusion. 

BIBLIOGRAPHY. 

Stokes,  W.:  Diseases  of  the  Heart  and  Aorta,  Dublin,  1854. 

Allbutt,  T.  Clifford:  The  Effect  of  Overwork  and  Strain  on  the  Heart  and  Great  Blood- 
vessels, St.  George's  Hosp.  Rep.  (Lond.),  1870,  v,  23. 

Da  Costa,  J.  M.:  On  the  Irritable  Heart;  a  Clinical  Study  of  a  Form  of  Functional  Cardiac 
Disorder  and  its  Consequences,  Am.  J.  M.  Sci.,  Phila.,  1871,  Ixi,  17.  Medical  Diagnosis, 
Phila.,  1864.  Also,  Observations  upon  Heart  Diseases  in  Soldiers,  etc.,  Mem.  U.  S. 
Sanitary  Commission,  Washington,  1867,  ch.  x,  p.  36. 

Maclean,  W.  C:  On  the  Diseases  of  the  Heart  in  the  British  Army  and  the  Remedy,  Brit. 
M.  J.,  Lond.,  1867,  i,  161. 

Myers,  A.  R.  B. :  Etiology  and  Prevalence  of  Diseases  of  the  Heart  among  Soldiers,  London, 
1870. 

Peacock,  T.  B.:  Lectures  on  Diseases  of  the  Heart,  Med.  Times  and  Gaz.,  Lond.,  1873, 
ii,  1,  57,  113,  169,  221,  319,  349.  On  Some  of  the  Causes  and  Effects  of  Valvular  Dis- 
eases of  the  Heart,  Lond.,  1865. 

Seitz,  Joh.:  Die  Ueberanstrengung  des  Herzens,  Berl.,  1875.  (A  monograph  by  the  author 
containing  translations  of  the  articles  of  Allbutt,  da  Costa,  and  Myers.) 

V.  Leyden,  E.:  Ueber  die  Herzkrankheiten  in  Folge  von  Ueberanstrengung,  Ztschr.  f. 
klin.  Med.,  Berl.,  1886,  xi,  105. 

Schott,  Th.:  Zur  acuten  Ueberanstrengung  des  Herzens  und  deren  Behandlung,  Wies- 
baden, 1898. 

Homung:  Beitrage  zur  Frage  der  acuten  Herzerweiterung,  Berl.  klin.  Wchnschr.,  1908, 
xlv,  1769. 

Henschen,  S.  E.:  Ueber  die  Herzdilatation  bei  Chlorose  und  Ansemie,  Mitth.  a.  d.  med. 
Khn.  zu  Upsala,  1898,  p.  27. 

Katzenstein,  J.:  Dilatation  und  Hypertrophic  des  Herzens,  Miinchen,  1903. 


II. 

PATHOLOGICAL  PHYSIOLOGY  OF  EXERCISE,  CARDIAC  OVER- 
STRAIN, HEART  FAILURE,  AND  COMPENSATION. 

PHYSIOLOGY    OF   EXERCISE. 

It  is  evident  from  the  foregoing  examples  that  muscular  efforts  which 
lead  to  cardiac  overstrain  are  in  themselves  merely  the  exaggeration  of 
ordinary  exercises.  To  understand  these  effects  it  is  necessary  first  to 
understand  those  of  ordinary  exercise. 

McCurdy  has  classified  exercises  as — 

1.  Exercises  of  speed,  like  running,  chest  weight  exercises,  etc.,  in  which 
the  individual  movements  require  little  effort,  but  the  main  effort  lies  in  the  rapidity  with 
which  they  are  repeated. 

2.  Exercises  of  endurance,  as  in  long-distance  running,  prolonged  walk- 
ing, forced  marches,  etc.,  in  which  the  movements  are  neither  difficult  nor  especially 
rapid  and  the  element  of  strain  sets  in  only  with  the  onset  of  fatigue. 

3.  Exercises    of   strain,    as  lifting  heavy  objects,  wrestling,  etc. 

Exercises  of  Speed. ^ — The  cases  of  cardiac  overstrain  reported  by  All- 
butt  and  da  Costa  represent  overstrain  from  exercises  of  endurance ;  those 
by  V.  Ley  den  and  Miinzinger  represent  exercises  of  strain. 

Masing,  Erlanger  and  Hooker,  Dawson  and  Eyster,  and  Gordon 
have  investigated  the  effect  of  exercises  of  speed  such  as  rapid  weight- 
lifting,  running,  etc.,  upon  man.  The  three  last  named  have  found  that 
in  individuals  in  training,  whose  circulation  is  least  affected,  mild  exercise 
causes  either  no  change  or  else  a  fall  of  blood-pressure.  Tangl  and 
Zuntz  also  found  this  in  horses  and  a  similar  period,  though  of  short 
duration,  in  dogs  running  on  a  tread -mill. 

In  all  muscular  work  an  increased  amount  of  CO3  is  given  off  from  the 
muscles  and  acts  as  a  hormone '  which  sets  into  play  the  following  physio- 
logical mechanisms: 

1.  Vasodilation  in  the  muscles,  diverting  four  or  five  times  as  much  blood  through 
this  channel   (Chauveau  and  Kaufmann). 

2.  Acceleration  of  the  heart,  at  first  through  diminution  in  the  vagus  action,  and  in 
the  later  stages  of  prolonged  severe  exercise  chiefly  through  stimulation  of  the  accelerators 
(Hering,  Bowen). 

3.  Vasoconstriction,  especially  in  the  splanchnic  vessels,  which  tends  to  counteract 
the  effect  of  the  vasodilatation  in  the  muscles. 

4.  Stimulation  of  the  augmentor  fibres,  and  perhaps  also  of  the  heart  muscle,  directly, 
causing  an  increased  force  of  contraction  (higher  maximal  pressure)  and  an  increased 
systolic  output  (higher  pulse-pressure).  Stimulation  of  the  augmentor  fibres  also,  as  a 
rule,  causes  increased  cardiac  tonicity. 

'  Hormone,  a  substance  generated  in  one  part  of  the  body  which  circulates  in  the 
blood,  reaches  and  sets  into  activity  another  organ,  thus  playing  the  role  of  a  "chemical 
messenger."  (Cf.  Starling,  E.  H.:  On  the  Chemical  Correlation  of  the  Functions  of  the 
Body,  Lancet,  Lond.,  1905,  ii,  391,  423,  501,  .579.) 

9  129 


130 


DISEASES    OF   THE    HEART    AND    AORTA. 


The  heart  of  the  trained  athlete  is  habitually  throwing  out 
an  amount  of  blood  suited,  not  to  the  needs  of  the  moment,  but  to  the 
needs  of  the  periods  of  exercise  to  which  he  has  accustomed  himself.  The 
systolic  output  is  above  normal  when  the  exercise  (and  hence  the  increased 
production  of  COj)  is  slight.  The  heart  is  thus  able  to  take  care  of  the 
excess  CO2  production  in  exercise  without  increasing  its  output;  and  hence 
the  vasodilatation  in  the  muscles  is  the  only  factor  influencing  the  blood- 
pressure.  When  the  exercise  becomes  severe  the  other  mechanisms  begin  to 
play  a  role. 

In  normal  but  not  trained  young  men  Masing  found 
that  upon  lifting  and  lowering  a  weight  with  the  feet  the  blood -pres- 
sure (maximal)  and  pulse-rate  rose  at  once  to  a  con- 
stant height,  where  they  remained  until  the  exercise 
ceased.     They  then  fell  almost  immediately  to  the  original  level.     The 


HSsb^BHHH 


BP 


^BHH 


EXERCISE  EXERCISE 

Fig.  113. — Alterations  of  blood-pressiire  due  to  rapid  lifting  of  light  weights  with  the  feet.     (After  Masing, 
DeiUsches  Arch.  f.  klin.  Med.,  vol.  Ixxiv.)    A.  Noimal  young  man.    B.  Man  aged  68. 

writer  has  found  that  the  minimal  pressure  rises  also,  but  less  than  the 
maximal,  the  pulse-pressure  being  increased.  In  middle-aged  persons 
Masing  found  that  the  pressure  rose  higher,  and  on  cessation  of  the  exercise 
required  several  minutes  to  reach  the  original  level;  while  in  very  old  persons 
the  rise  was  still  greater  and  neither  pressure  nor  rate  returned  to  normal 
for  a  considerable  period.    The  response  is  proportional  to  the  effort. 

When  exercise  is  continued  in  normal  young  persons  and 
the  organism  readapts  itself  to  the  effort  (the  "second  wind"  setting  in), 
blood-pressure  and  pulse-pressure  again  fall  to  a  fairly  constant  level 
(Dawson  and  Hatfield).  This  probably  explains  why  the  heart-rate  of 
well-trained  Marathon  racers  is  sometimes  slow  at  the  finish.  In  animal 
experiments  it  finds  its  analogy  in  the  improved  cardiac  action  observed 
as  a  result  of  clamping  the  thoracic  aorta,  and  represents  the  response  of 
the  heart  to  a  strain  which  is  not  excessive. 

The  weaker  the  individual  or  the  more  severe  the 
exercise  the  more  prominent  become  factors  2,  3,  and 
4,  the  greater  the  rise  of  bloo  d-p  ressure  an«i  the 
greater  the  pulse-rate.  The  slowness  at  w^hich  conditions  return 
to  normal  is  more  or  less  proportional  to  the  exertion  and  the  fatigue. 

It  is  also  true  that  for  a  given  amount  of  exercise  performed  in  a  given 
time  the  amount  of  CO,  formed  is  least  when  it  is  done  with  least  effort 
by   trained   individuals  and  increases  when  the  effort  becomes  marked. 


PHYSIOLOGY  OF   EXERCISE. 


131 


Zuntz  and  Schumburg  have  shown  upon  German  soldiers  that  a  certain 
short  march  used  up  only  554.8  calories  of  energy  when  the  subjects  were 
fresh,  but  required  635.5  calories  when  they  were  fatigued.  This  is  prob- 
ably due  to  the  fact  that  with  the  increase  in  effort  accessory  muscles  are 
called  into  play,  many  of  which  contract  and  give  off  CO2  without  mate- 
rially improving  the  execution  of  the  exercise. 


MINUTES 
PULSE             2          it 

.       8      10      12      14      16      18          1 

170| 

160   -^ 
150i  — 

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s 

^ 

s^ 

'^ 

s 

— 

► — 

'^A(\ 

s 

0 

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■ 

s 

■ 

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8 

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7 

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8 

Fig.  114. —  Effect  of  walking  on  a  level  on 
patient  with  badly  broken  compensation.  (After 
Cabot  and  Bruce,  Am.  J.  M.  Sc,  cxxxiv.) 


Fig.  115. — Effect  of  prolonged  exercise  upon 
the  blood-pressure  of  men  in  various  degrees  of 
muscular  strength.  The  arrows  indicate  the  point 
at  which  symptoms  of  exhaustion  set  in.  COM- 
PENSATED, compensated  heart  lesions;  FAIL- 
ING, broken  compensation  with  heart  failure. 


Exercises  of  Endurance.  —  The  point  at  which  an  exercise  of  speed 
becomes  converted  into  an  exercise  of  endurance  is  more  or  less  relative 
and  depends  chiefly  upon  the  condition  and  the  training  of  the  individual. 
The  most  typical  exercises  of  endurance,  the  forced  march,  the  long-dis- 
tance runs  (Marathon  races),  and  long-distance  bicycle  races,  have  been 
carefully  studied  by  Zuntz  and  Schumburg,  Blake  and  Larrabee,  Dietlen 
and  Moritz,  and  R.  T.  Abercrombie.  In  these  exercises  the  least  changes 
occur  in  the  best-trained  individuals  in  whom  the  amount  of  effort  put 
forth  is  least  or  least  prolonged. 

The  pulse-rate  of  the  men  who  finished  in  the  Marathon  races  at  Boston  showed  sur- 
prisingly little  increase,  the  greatest  rise  during  the  race  of  1900  being  from  76  before  to 
144  after;  but  the  average  rate  after  the  race  was  103  (Blake  and  Larrabee).  There  was 
frequently  a  moderate  grade  of  irregularity.  Zuntz  and  Schumburg  found  similar  effects. 
The  blood-pressure  after  the  race  was  usually  found  to  be  a  trifle  lower  than  before  the 
start,  though  it  varied  greatly  in  different  individuals.  J.  Barach  has  recently  obtained 
similar  results  with  the  Erlanger  apparatus  upon  another  set  of  trained  Marathon  racers. 
The  orthodiagraph  showed  dilatation  of  the  heart  in  all  his  cases.  Quite  different  are 
the  results  in  long-distance  races  run  by  amateurs.  Dr.  R.  T.  Abercrombie  has  recently 
made  a  careful  study  of  the  condition  of  contestants  in  a  twenty-mile  road  race  before 
and  immediately  after  the  race.  Before  the  race  the  average  blood-pressures  with  the 
Erlanger  apparatus  were:  maximal  120-130,  minimal  75-80;  pulse-rate  80.  Immediately 
after  the  race  the  pulse  was  in  almost  every  instance  too  feeble  to  be  counted,  as  were 
also  the  heart  sounds;  and  neither  these  nor  the  blood-pressure  could  be  satisfactorily 
estimated  until  one-half  hour  after  the  finish,  when  the  pulse-rate  was  usually  about  120 
per  minute,  the  maximal  pressure  about  75-100  mm.  Hg.     The  heart  sounds  were  still 


132 


DISEASES   OF   THE   HEART   AND    AORTA. 


rapid  and  feeble.  Nevertheless  all  of  these  men  felt  quite  well,  and  were  able  to  enjoy  a 
cold  plunge  immediately  after  the  examination.  Within  an  hour  after  the  finish  they 
were  all  feeling  quite  active.  The  blood-pressure  was  usually  found  to  be  lower  than  be- 
fore the  start,  but  this  varied  greatly  in  individual  cases. 

Not  all  the  results  of  endurance  tests  are  as  mild  as  these.  During  the  amateur 
athletic  contests  in  the  United  States  the  past  five  years  there  have  been  several  cases  of 
permanent  heart  failure  following  directly  upon  overstrain  in 
long-distance  runs.  As  in  da  Costa's  series,  the  persons  whose  hearts  were  injured 
were  usually  boys  under  twenty  who  were  poorly  trained  and  whose  hearts  were  not  fitted 
for  the  strain  put  upon  them. 

As  regards  the  metabolism  during  such  exercise  Zuntz  and  Schumburg,  and  also  A. 
Loewy  and  L.  Zuntz,  found  that  both  the  amount  of  CO2  given  off  per  minute  and  the 
respiratory  quotient  were  markedly  lessened  (COj  falling  from  802.3  c.c.  to  743.0  c.c.  per 
minute;  respiratory  quotient  falling  from  0.855  to  0.780)  at  the  end  of  the  exertion,  though 
the  O,  used  was  unchanged.  This  is  due  to  formation  of  intermediate  oxidation  prod- 
ucts; sarcolactic  acid,  /?-oxybutyric  acid,  etc.,  the  pressure  of  whose  salts  may  add  to 
the  fatigue.  Moreover,  the  lessened  output  of  CO2  indicates  a  low  CO2  content  of  the  blood 
(acapnia),  and,  as  Henderson  has  shown,  this  in  turn  causes  dilatation  of  the  veins  and 
causes  the  blood  to  gradually  leave  the  arteries,  stagnate  in  the  venous  reservoir  (see 
page  31),  and  thus  diminish  the  rapidity  of  the  blood  flow. 

Corresponding  to  the  variations  in  rapidity  of  blood  flow,  the  urine 
is  increased  in  amount  during  mild  exercise,  decreased  during  severe  exer- 
cise.   After  boat  races  and   after  the  Marathon  races  it  often  contains 

albumin,  casts,  and  even  traces  of 
blood,  probably  as  a  result  of  stasis 
or  high  pressure  in  the  renal  veins 
and  capillaries. 

Exei'cise  of  Strain. — The  effect  of 
exercises  of  strain,  lifting,  etc.,  is  totally 
different.  McCurdy,  Bruck,  and  others 
have  shown  that  these  exercises  cause 
a  far  greater  rise  of  blood-pressure  than 
do  the  exercises  of  speed;  and,  on  the 
other  hand,  the  pulse-rate  does  not  rise 
rapidly  but  is  at  first  either  slowed  or 
unchanged.  The  rise  in  blood-pressure 
is  greater  in  arteriosclerotics,  old  per- 
sons, and  weak  individuals  for  the 
same  amount  of  work  than  in  well- 
developed  normal  individuals.  In  per- 
sons already  suffering  from  broken 
compensation,  on  the  other  hand,  the 
heart  absolutely  fails  to  respond  with 
increased  effort,  and  may  be  so  greatly 
weakened  by  the  strain  that  the  blood- 
pressure  may  fall. 
All  the  factors  which  are  called  into  play  by  the  hormone  action  of  CO, 
in  exercises  of  speed  and  of  endurance  are  also  acting  in  exercises  of  strain; 
but,  since  the  latter  are  usually  intermittent  or  of  short  duration,  their 
effects  are  at  first  overshadowed  by  others  which  are  more  intense. 

In  carrying  out  any  exercise  involving  muscular 
strain   the   individual   involuntarily    closes  his    glottis 


Fig.  116. — Rise  of  blood -pr&ssu re  during 
Valsalva's  experiment  and  during  exercise. 
Normal  individual.  (Schematic,  after  Bruck.) 
ARTERJOSCLER,  curve  of  blood-pressure  in 
man  with  arteriosclerosis  performing  the  same 
exercise. 


PHYSIOLOGY  OF  EXERCISE.  133 

and  executes  an  attempt  at  forced  expiration.  The 
result  of  this  is  a  tremendous  increase  in  intrathoracic  pressure,  which 
hinders  the  outflow  of  bood  from  the  right  ventricle  as  well  as  the  inflow 
into  the  right  auricle. 

The  result  of  these  two  factors  is  dilatation  of  the  right  ventricle  and  stasis  in  the 
systemic  veins,  which  is  still  further  shown  by  the  cyanosis  of  the  face  and  distention  of  the 
veins  that  accompany  all  such  exercises  even  in  trained  athletes.  The  venous  stasis  is 
further  increased  by  the  sudden  squeezing  out  of  blood  from  the  large  masses  of  skeletal 
muscles,  which  are  being  forcibly  contracted  simultaneously,  as  well  as  from  the  vessels 
of  the  splancluiic  area. 

The  high  pressure  within  the  lungs  stimulates  the  sensory  endings  of  the  vagus,  which 
in  turn  reflexly  stimulate  the  motor  nucleus  of  the  vagus  and  the  vasomotor  centre  in  the 
medulla  and  cause  both  slowing  of  the  pulse  and  rise  of  blood-pressure.  The  general  result 
is  the  same,  but  less  marked  when  the  Valsalva  experiment  only  (forced  expiration  with 
glottis  closed)  is  carried  out,  and  depends  very  largely  upon  this  factor. 

SIZE    OF    HEART    AFTER    EXERCISE. 

Diminution  in  Size  in  Healthy  Hearts.  —  Examined  with  the  X-ray 
the  auricles  are  seen  to  dilate  greatly,  but  the  ventricles  do  not,  as  a  rule, 
show  any  dilatation  Avhatever.  This  again  is  a  question  of  tonus,  and  here 
also  the  latter  factor  seems  to  determine  whether  dilatation  shall  set  in 
or  not.  All  exercises  when  sufficiently  severe  lead  to  dilatation  of  hearts 
whose  myocardium  has  suffered  injury,  especially  during  the  course  of 


Fig.  117. — Semi-schematic  drawing  showing  variations  in  size  of  the  heart  of  a  long-distance 
bicycle  rider,  as  the  result  of  a  very  long  race;  reconstructed  from  the  orthodiagrapliic  outline.  A.  Before 
the  race.  B.  Immediately  after  the  race,  showing  the  great  diminution  in  size  of  the  heart.  C.  Four 
weeks  later.     (After  Moritz  and  Dietlen,  Munchen  med.  Wchnschr.,  1908,  Iv.) 

infectious  diseases  (da  Costa,  Zuntz  and  Schumburg,  de  la  Camp,  Moritz 
and  Dietlen)  or  during  the  first  few  weeks  following  them.  On  the  other 
hand,  Schott  has  claimed  to  have  seen  cardiac  dilatation  in  healthy  wrestlers 
and  bicycle  riders  as  a  result  of  short  .wrestling  bouts.  This  fact  has  been 
disputed  by  a  number  of  observers  who  have  carefully  controlled  the  more 
or  less  subjective  findings  of  percussion  by  outlining  the  heart  with  the 
orthodiagraph. 

The  following  exercises  have  been  studied:  bicycle  riding,  by  Mendelsohn,  Albu, 
Beyer,  Schieffer,  Dietlen  and  Moritz;  marching,  by  Zuntz  and  Schumburg,  Albu  and 
Caspari,  Balders,  Heichelheim  and  Metzger;  football  playing,  by  F.  Pick  and  by  Selig; 
ski  running,  by  Henschen;  wrestling,  by  Levy-Dorn,  Selig,  Mendl  and  Selig;  swimming, 
by  Kienbock,  Selig  and  Beck. 

The  results  of  these  observations  quite  uniformly  confirm  those  of 
de  la  Camp  in  showing  that  exercise,  even  to  the  point  of  exhaustion  and 


134  DISEASES   OF   THE    HEART    AND    AORTA. 

fainting,  does  not  bring  about  cardiac  dilatation  in  otherwise  healthy  men. 
In  most  cases  the  X-ray  and  orthodiagraph  show  an  actual  diminution  in 
the  volume  of  the  heart  *  (see  Fig.  117).  De  la  Camp  also  found  that  healthy 
dogs  could  run  upon  a  tread-mill  until  they  dropped  from  exhaustion  with- 
out causing  dilatation  of  the  heart;  w^hereas  the  hearts  of  dogs  which  had 
been  poisoned  with  phosphorus  and  which  were  in  a  state  of  mild  fatty 
degeneration  dilated  greatly  from  the  same  exercise. 

Dilatation  and  Myocardial  Injury.  —  On  the  other  hand,  Hornung, 
who  has  watched  the  course  of  1100  cases  of  weak  heart  with  the  X-ray, 
states  that  in  such  persons  acute  dilatations  (demonstrable  with  the  ortho- 
diagraph) are  very  common  as  the  result  of  slight  overstrain.  It  may 
require  comparatively  little  strain  to  bring  this  about.  For  example,  he 
cites  the  case  of  a  woman  with  a  weak  heart  who  acquired  a  dilatation  by 
taking  a  short  cut  instead  of  a  gradual  ascent  while  climbing  a  hill  (Oertel's 
Terrainkur).  The  dilatation  lasted  for  several  days  and  gradually  passed 
off.  Persons  whose  hearts  are  in  this  labile  equilibrium  are  liable  to  have 
repeated  attacks.  But  the  cardiac  condition  rarely  stands  still.  It  grad- 
ually becomes  either  better  or  worse,  according  to  the  treatment  and  the 
mode  of  life  of  the  patient. 

Thoracic  and  Abdominal  Constriction  as  a  Factor  in  Cardiac  Over= 
strain.  —  A  high  diaphragm  due  to  tight  belts  or  corsets  is  one  of  the  most 
important  factors  which  predispose  to  cardiac  overstrain.  This  was  already 
shown  by  A.  R.  B.  Myers  in  1867.  Myers  observed  that  certain  cavalry 
regiments  in  the  Indian  Army  were  particularly  subject  to  cardiac  over- 
strain and  to  chronic  cardiac  disease,  even  more  so  than  the  infantry  regi- 
ments which  were  doing  more  arduous  work  under  the  same  conditions  of 
climate  and  diet.  He  noticed  that  the  uniforms  of  this  cavalry  regiment 
were  very  tightly  belted  and  had  tight  cuirasses  compressing  the  chest. 
Upon  experimentation  he  found  that  the  men  in  this  regiment,  when  not 
wearing  their  uniforms,  were  quite  as  strong  as  those  of  other  regiments 
in  the  service.  He  also  found  that  the  same  men  were  able  to  withstand 
much  greater  exertion  in  the  same  uniforms  if  only  the  belts  were  worn 
looser.  This  has  been  shown  with  somewhat  greater  exactness  by  Th. 
Schott.  Schott  demonstrated  with  the  orthodiagraph  that  wrestlers  could 
withstand  much  greater  exertion  before  the  onset  of  acute  dilatation  or  of 
cardiac  symptoms  if  they  wore  no  belts  than  if  they  were  tightly  belted. 
This  is,  of  course,  not  surprising,  and  is  simply  another  way  of  demonstrat- 
ing the  every-day  experience  of  most  healthy  women  that  they  can  do 
more  work  without  a  corset  or  with  a  loose  one  than  when  wearing  one 
that  is  tightly  laced. 

The  reason  for  this  is  twofold.  The  belt  interferes  with  the  respira- 
tory movements  of  the  abdomen  and  diaphragm,  and  hence  diminishes  the 
rhythmic  alternation  of  positive  and  negative  pressures,  of  force-pump  and 
suction-pump  action,  in  one  of  the  largest  of  the  vascular  reservoirs,  thus 

'  The  syncope  (cerebral  anaemia)  under  these  conditions  is  probably  due  to  the  exactly 
opposite  condition,  diminished  cardiac  filling  and  hence  diminished 
cardiac  output;  arterial  anaemia  due  to  rapid  pulse-rate  in  a  heart  whose  tonicity 
is  increased.  (This  condition  is  fully  discussed  in  the  chapters  on  Paroxysmal  Tachycardia 
and  Miscellaneous  Heart  Diseases.) 


PHYSIOLOGY  OF   EXERCISE. 


135 


diminishing  the  rapidity  of  blood-flow.  Moreover  the  viscera  are  pushed 
back  and  the  diaphragm  is  pushed  upward  by  the  belt,  and  this  causes  the 
heart  to  assume  a  more  transverse  position,  in  which  kinking  of  the  great 
veins,  the  aorta,  and  the  pulmonary  artery  sets  in,  and  both  the  filling  and 
the  emptying  of  the  heart  are  impeded.  This  mechanism  is  readily  demon- 
strated upon  the  exposed  heart  of  the  living  animal.  A  comparatively 
slight  upward  or  downward  displacement  of  the  heart  from  its  natural  posi- 
tion may  cause  tremendous  fall  in  blood-pressure  and  interference  with 
the  work  of  the  heart. 

PHYSIOLOGICAL   FACTORS    BRINGING    ABOUT    DILATATION. 

The  diminution  in  the  size  of  the  heart  which  was  found  so  uniformly 
by  the  above-mentioned  observers  seems  to  be  due,  in  part,  to  diminished 
filling  of  the  ventricles  when  the  heart  is  rapid,  but  chiefly  to  the  fact  that 
the  cardiac  tonicity  was  increased  by  the  strain.*  This  clinical  observa- 
tion has  its  analogue  in  experimentation  on  animals.  O.  Frank  has  shown 
that,  other  things  being  equal,  a  moderate  increase  in  intraventricular 
pressure  acts  as  a  stimulus  and  causes  an  increase  in  the  force  of  the  next 
beat.     If  the  pressure  is  raised  further  it  reaches  an  optimum;  but  if  it 


VOL. 


B.  p. 


Fig.  118. —  Effect  of  strain  upon  the  dog's  heart  whose  tonicity  is  good.  Volume  curve  (VOL.) 
and  blood-pressure  curve  (B.P.)  of  an  animal  whose  heart  is  in  good  condition.  Descending  thoracic 
aorta  clamped  at  the  moment  indicated  by  the  arrow.  Momentary  dilatation  followed  by  a  diminution 
in  size.  The  heart  becomes  smaller  than  before  the  clamping.  Tonicity  is  increased  {T  +).  Blood- 
pressures  maximal  and  minimal  are  also  increased. 

becomes  too  high  the  force  of  contraction  becomes  much  weaker  than  if 
there  were  no  load  at  all.  There  is  a  similar  effect  upon  cardiac  tonicity. 
Hirschfelder  has  shown  that  if  the  thoracic  aorta  of  the  dog  is  clamped  the 
ventricles  at  first  dilate  rapidly  and  the  systolic  output  diminishes.  If  the 
heart  is  in  good  condition  the  systoles  soon  begin  to  increase,  the  excess 
of  blood  is  pumped  out  of  the  ventricular  cavities  in  systole,  and  on  the 
other  hand,  in  spite  of  the  high  pressure  in  the  veins,  less  blood  enters  the 
ventricles  than  before. 

'  It  is  possible  that  acapnia  (page  31)  may  play  a  role  under  these  conditions. 


136  DISEASES   OF   THE   HEART    AND    AORTA. 

The  amount  of  blood  which  enters  the  ventricles  depends  upon  two 
factors:  1.  As  Howell  and  Donaldson  have  shown  for  the  excised  heart, 
and  Roy  and  Adami  for  the  dog's  heart  in  situ,  it  is  more  or  less  propor- 
tional to  the  venous  or  intra-auricular  pressure.  2.  Roy  and  Adami, 
Hirschfelder,  Cameron,  and  others  have  shown  that  it  is  also  dependent 
upon  the  cardiac  tonicity,  being  greater  when  tonicity  is  low  (dilatation) 
and  least  when  tonicity  is  high.  It  is  therefore  evident  that  a  heart  whose 
tonicity  is  high  will  withstand  a  comparatively  high  venous  pressure  with- 
out dilating,  whereas  when  the  tonicity  is  low  it  readily  overfills. 

Several  factors  contribute  toward  diminishing  the  strength  of  an  over- 
filled heart:  1.  With  the  increase  of  the  cubical  contents  and  the  internal 
surface  of  the  ventricles  the  mechanical  work  necessarv  to  exert  a  normal 


VOL. 


B.  p. 


SEC. 

Fig.  119. — Volume  curve  of  a  dog  whose  cardiac  tonicity  is  low.  Clamping  the  aorta  is  followed 
by  permanent  dilatation  and  only  a  !<light  momentary  increase  in  blood-pressure.  The  systolic  output 
is  diminished,  owing  to  inability  of  the  heart  to  force  the  usual  quota  of  blood  against  the  increased 
resistance. 

pressure  is  increased  (Roy  and  Adami).  2.  In  the  dilated  heart  the  blood 
flow  through  the  coronary  arteries  and  hence  the  nutrition  of  the  cardiac 
walls  is  diminished  (Hyde).  Moreover  the  dilatation  of  the  ventricles  may 
or  may  not  be  permanent,  dependent  upon  the  tonus  of  the  heart  muscle 
(Hirschfelder,  Cameron).  If  the  latter  is  low  the  dilatation  remains  and 
increases,  whereas  if  it  is  high  the  increased  pressure  acts  as  a  stimulus. 
It  is  usually  a  high  venous  pressure  which  keeps  the  heart  dilated  and  a 
low  tonicity  which  permits  it  to  remain  so. 

Since  the  venous  pressure  is  certainly  highest  in  the  exercises  of  strain, 
it  is  not  surprising  that  permanent  heart  trouble  arising  in  previously 
healthy  persons  as  a  result  of  primary  cardiac  overstrain  is  particularly 
common  among  persons  (butchers,  porters,  stevedores,  etc.)  who  lift  the 
heaviest  weights. 

EFFECT    OF    THE    STRAIN    UPON    THE    HE.\RT. 

The  response  of  the  heart  to  a  muscular  exertion  which  ju.st  fatigues 
may  be  of  three  grades:  1.  The  heart  becomes  smaller  or  the  cardiac 
outlines  are  unchanged — tonicity  high  (normal  hearts).  2.  There  is  a 
tran.sitory  dilatation  (after  acute  infections  and  in  hearts  with  myocardial 
or  some  other  cardiac  disturbance).  3.,  The  overstrain  leads  to  perma- 
nent injury  of  the  heart,  often  with  permanent  arrhythmia  (chronic  car- 


PHYSIOLOGY  OF   EXERCISE. 


137 


diac  overstrain,  myocardial  changes).  These  three  conditions  find  their 
analogues  in  the  effects  of  clamping  the  thoracic  aorta  upon  the  volume 
of  the  ventricles  (Fig.  119). 

As  has  been  seen  in  the  cases  quoted  above,  the  repetition  of  the  strain 
is  quite  as  important  a  factor  in  heart  failure  as  is  the  overstrain  itself. 
Even  a  heart  with  extremely  low  tonicity  will,  in  most  cases,  recover  and 
gradually  return  to  normal  volume  after  the  strain  has  been  removed,  but 
during  the  period  when  it  is  still  dilated  it  is  much  more  susceptible  to  a 
further  overstrain.  On  the  other  hand,  after  a  sufficient  period  of  rest  it 
regains  its  former  volume  and  still  later  its  former  tonicity,  and  once  more 
reaches  its  original  strength.  That  this  is  probably  the  case  in  man  also  is 
shown  by  the  fact  that  Poynton  did  not  regard  an  occasional  overstrain 


1 

AO 

CL 

2 
3 

-r 

fc^ 

"^^^^^^ 

Fig.  120. — Effect  upon  the  volume  of  the  dog's  heart  produced  by  clamping  the  descending  tho- 
racic aorta.  Ascent  of  curve  =  diminution  in  volume;  descent  =  dilatation.  1,  normal  and  vigorous  heart; 
2,  slightly  weakened  heart  with  diminished  tonicity;  3,  very  weak  heart  with  much  diminished  tonicity. 


as  of  any  special  significance  in  boys,  provided  it  were  followed  by  a  period 
of  sufficient  rest.  Moreover,  Meylan  has  found  that  the  lives  of  oarsmen 
upon  the  Harvard  boat-crews  were  somewhat  longer  than  the  average  for 
normal  individuals,  in  spite  of  the  fact  that  albuminuria  and  other  signs 
of  cardiac  overstrain  are  quite  common  just  after  such  races.  Indeed 
not  a  single  case  of  cardiac  disease  developed  among  the  152  oarsmen 
of  his  series,  which  comprised  members  of  the  intercollegiate  crews  from 
1852  to  1892.  There  was  only  one  case  in  which  enlargement  of  the  heart 
was  noted  and  one  case  of  irregularity,  but  neither  of  these  inconvenienced 
the  patient. 

These  individuals,  in  contrast  to  cases  like  that  of  v.  Leyden,  had  rested 
sufficiently  between  the  periods  of  strain,  and  the  second  strains  had  not 
been  imposed  upon  their  hearts  until  long  after  their  strength  and  tonicity 
had  returned  to  normal.    In  v.  Leyden's  case  and  other  cases  of  permanent 


138  DISEASES   OF   THE    HEART    AND    AORTA. 

heart  failure,  the  heart  was  still  dilated  at  the  time  of  renewed  strain.  This 
condition  seems  to  determine  the  border-line  between  heart  failure  and 
recovery. 

The  border-line  conditions  may  therefore  be  summarized  as  follows: 
Dilatation  of  the  heart  during  or  after  exercise  represents  a  pathological, 
though  not  a  very  infrequent,  condition  in  which  the  heart  has  overstepped 
its  limits.  The  condition  usually  recedes  and  leaves  no  traces  unless  the 
heart  is  again  overstrained  while  still  in  a  dilated  condition. 

As  regards  the  anatomical  changes  induced  by  the  condition  of  over- 
strain, Roy  and  Adami  have  shown  that,  when  the  dog's  heart  begins  to 
fail  after  clamping  the  aorta,  stasis  occurs  in  the  coronary  veins  and  the 
heart  muscle  becomes  oedematous.  This  oedema  is  especially  marked  in 
the  regions  which  are  richest  in  connective  tissue,  the  auricles  and  the 
auriculoventricular  valves.  They  believe  that  when  the  strain  is  con- 
tinued the  oedema  is  replaced  by  infiltration,  the  infiltration  by  connective 
tissue,  and  that  fibrous  myocarditis  results.  Indeed,  a  fibrous  myocarditis 
(cardiosclerosis)  is  a  common  autopsy  finding  in  cases  of  long-continued 
cardiac  overstrain  in  which  there  has  been  no  severe  infectious  disease  to 
account  for  the  lesion.  On  the  other  hand,  Pearce  and  Fleisher  and  Loeb 
have  found  exactly  the  stages  mentioned  by  Roy  and  Adami  in  animals  in 
the  various  stages  of  adrenahn  myocarditis  (see  page  226) . 

BROKEN   CARDIAC   COMPENSATION. 

As  long  as  the  heart  is  able  to  maintain  a  certain  velocity  of  blood 
flow  throughout  the  circulation,  the  latter  may  be  said  to  be  compensated  ; 
but  when  the  blood  stagnates  to  such  a  degree  as  to  give  rise  to  the  signs 
and  symptoms  of  stasis,  compensation  may  be  said  to  be  broken. 

There  are  two  forms  of  broken  compensation.  When  the  blood  stag- 
nates in  the  systemic  veins  from  failure  of  the  right  side  of  the  heart,  the 
condition  may  be  termed  broken  systemic  compensation; 
when  stasis  occurs  in  the  lungs  because  the  left  side  of  the  heart  is  not 
acting  as  strongly  as  the  right,  broken  pulmonary  compensation 
results.  Each  of  these  two  forms  brings  with  it  a  characteristic  group  of 
symptoms:  The  broken  systemic  circulation  (usually  designated  simply  as 
"  broken  compensation  ")  manifests  itself  in  the  signs  and  symptoms  which 
are  seen  in  tricuspid  insufficiency — breathlessness,  cyanosis,  oedema,  begin- 
ning in  the  feet  and  legs,  enlargement  of  the  liver,  and  systolic  pulsation 
of  the  liver  and  veins,  etc.  Broken  pulmonary  compensation  is  accom- 
panied by  the  signs  and  symptoms  of  an  acute  severe  mitral  insufficiency — 
intense  respiratory  disturbance,  dyspnoea,  cough,  occasionally  pulmonary 
hemorrhage,  and  the  sputum  containing  the  characteristic  cells  of  passive 
congestion  (Herzfehlerzellen). 

Broken  Systemic  Compensation.— From  the  physiological  stand-point, 
the  cardinal  features  of  broken  systemic  compensation  are  dilatation  and 
weakening  of  the  right  ventricle,  dilatation  and  paralysis  of  the  right 
auricle,  increase  n  COj  and  decrease  in  O2  in  the  venous  blood,  functional 
insufficiency  of  the  tricuspid  valve,  rise  in  venous  pressure  (often  to  as 
high  as  20  mm.  Hg)  (Fig.  121,  III).  The  signs  are  cyanosis,  engorgement 
and  systolic  pulsation  of  the  veins,  enlargement  of  the  liver,  oedema  of  the 


BROKEN   CARDIAC   COMPENSATION. 


139 


feet  and  legs,  and  sometimes  venous  stasis  in  the  medulla,  vasoconstriction, 
high  blood-pressure,  and  dyspnoea  of  medullary  origin. 

Broken  Pulmonary  Compensation. — The  characteristics  of  broken  pul- 
monary compensation  are  dilatation  and  weakening  of  the  left  ventricle, 
•dilatation  and  usually  paralysis  of  the  left  auricle,  rise  of  pressure  and 
stasis  in  the  pulmonary  veins,  engorgement  of  the  pulmonary  capillaries, 
and  "erection"  of  the  lung  tissue  (v.  Basch)  (Fig.  121,  IV).  Welch  has 
shown  that  when  the  stasis  is  very  intense,  pulmonary  oedema  sets  in. 
V.  Basch  and  his  pupils  have  applied  this  idea  to  the  milder  pulmon- 
ary manifestations  and  have  shown  that  a  moderate  erection  of  the  lung 
tissue  brings  on  cardiac  dyspnoea  and  leads  to  bronchitis  and  cough.  His 
pupil,  Kauders,  has  shown  that  the  position  of  the  diaphragm  is  affected 
refiexly  by  the  amount  of  blood  in  the  lungs,  congestion  causing  the 
diaphragm  to  descend,  depletion  causing  it  to  ascend.  It  is  thus  usually 
lower  than  normal  in  mitral  lesions,  higher  in  pulmonary  and  tricuspid. 


NORMAL 


II 

BROKEN 

PULMONARY 

COMPENSATION 


III 

BROKEN 

SYSTEMIC 

COMPENSATION 


IV 

FAILURE  OF 

BOTH 
VENTRICLES 


Fig.  121. —  Diagram  showing  changes  in  the  circulation.  I,  normal;  II,  broken  pulmonary  com- 
pensation; III,  broken  systemic  compensation;  IV,  both  compensations  fail;  stases  in  lungs  and  veins. 
AO,  pressure  in  the  aorta,  PA. 


V.  Basch  also  believed  that  the  congestion  of  the  lungs  causes  the  elastic- 
ity of  the  lungs  to  diminish  and  to  become  so  rigid  as  actually  to  diminish 
the  respiratory  expansion,  but  the  experiments  of  D.  Gerhardt  have  thrown 
■doubt  upon  this  phase  of  his  conclusions.  As  regards  the  changes  of  pres- 
sure and  the  distribution  of  the  blood,  however,  v.  Basch.'s  conclusions 
have  been  confirmed,  not  only  by  Gerhardt  in  Germany  but  by  W.  G. 
MacCallum  and  McClure  in  America. 

In  badly  weakened  hearts  both  forms  of  broken  compensation  may 
be  present,  sometimes  features  of  one,  sometimes  of  the  other,  predomi- 
nating. 

Functional  Valvular  Insufficiency  in  Broken  Compensation. — Although 
it  has  not  been  absolutely  proved,  it  seems  almost  certain  that  the  occur- 
rence of  broken  compensation  from  acute  dilatation  is  accompanied  by  a 
functional  insufficiency  of  the  tricuspid  or  the  mitral  orifice  which  may 
be  of  transitory  duration.  Indeed  this  functional  insufficiency  of  the  tri- 
cuspid valve  in  heart  failure  is  much  more  common  than  organic  lesion  of 


140  DISEASES   OF   THE   HEART    AND    AORTA. 

the  valve,  and  in  long-standing  cases  is  accompanied  by  actual  stretch- 
ing of  the  tricuspid  orifice  (T.  W.  King,  G.  A.  Gibson,  Mackenzie,  Keith). 

T.  W.  King,  in  1837,  demonstrated  that  such  functional  insufficiencies 
occur  at  the  triscupid  valves,  and  even  that  they  were  dependent  upon  the 
tonicity  of  the  ventricular  fibres;  since  the  valves  which  had  been  in- 
sufficient a  few  hours  after  death  held  water  perfectly  after  rigor  mortis 
had  set  in  (quoted  in  full  on  page  396).  These  observations  have  been 
confirmed  and  extended  by  G.  A.  Gibson,  Frangois-Franck,  Mackenzie, 
Friedreich,  Marey,  Hirschfelder,  Keith.  Hering  demonstrated  the  same 
phenomenon  for  the  mitral  valve  in  rabbits,  but  found  that  in  dogs  the 
mitral  valve  did  not  leak  even  after  clamping  the  aorta.  Stewart  and  the 
writer  have  been  able  to  demonstrate  the  occurrence  of  such  an  insuffi- 
ciency of  the  mitral  valve  when  the  aorta  was  clamped,  in  dogs  whose 
aortic  valves  had  been  rendered  insufficient.  In  man  Morton  Prince  and 
Broadbent  have  noted  the  presence  of  transitory  mitral  systolic  murmurs 
(sometimes  transmitted  to  the  axilla)  in  men  who  were  being  subjected 
to  the  strain  of  civil  service  examinations,  and  in  cases  with  similar  signs 
Minkowski  has  obtained  tracings  from  the  oesophagus  which  have  the  form 
characteristic  of  mitral  insufficiency. 

In  the  earlier  stages  of  cardiac  overstrain  the  dilatation  of  the  auricles 
is  a  more  or  less  passive  phenomenon  which  exerts  little  influence  upon  the 
circulation,  but  in  the  more  severe  stages  it  may  play  a  leading  role. 

Auricular  Paralysis  and  Arrhythmia  in  Cardiac  Overstrain.  —  Condi- 
tions which  affect  tonicity  and  filling  of  the  ventricles  have  a  still  greater 
effect  upon  the  tonicity  and  filling  of  the  auricles.  It  was  demonstrated 
by  Ludwig's  pupils.  Waller  (1878)  and  v.  Frey  and  Krehl  (1890),  that 
when  the  ventricles  began  to  fail,  the  auricles  soon  became  overloaded 
with  blood  and  ceased  to  contract  entirely  when  the  pressure  reached 
15-20  mm.  Hg.  As  a  rule  this  does  not  affect  the  cardiac  rhythm,  but 
Hirschfelder  has  shown  in  dogs  that  when  this  is  brought  about  by  nar- 
rowing the  mitral  orifice;  an  absolute  irregularity  (disorderly  rhythm) 
may  set  in  without  any  apparent  contractions  carried  out  by  the  auricles. 

It  seems  probable  that,  under  these  circumstances,  the  contraction  stimuli  originate 
in  the  auricle  and  are  transmitted  but  are  not  carried  out  by  these  chambers;  just  as 
Biedermann  has  shown  that  muscle  in  water  rigor  can  originate  and  transmit  a  stimulus 
without  itself  contracting.  Mackenzie  and  others  beheve  that  under  these  circumstances 
the  stimulus  no  longer  originates  in  the  sinus  portion  of  the  auricle  but  in  the  Purkinje 
cells  of  the  His  bundle  (at  Tawara's  nodal  point,  Knotenpunkt),  and  hence  designates 
this  absolute  irregularity  as  nodal  rhythm.  They  believe  that  the  auricle  and  ventricle 
are  contracting  simultaneously  under  these  circumstances.  Since  Retzer  has  traced  the 
bundle  directly  into  the  sinus  region  and  believes  that  there  is  no  nodal  point,  this  view 
seems  open  to  question. 

Arrhythmia. — Whatever  may  be  the  origin  of  the  arrhythmia  it  is  very  common  in 
severe  overstrains.  This  not  infrequently  arises  in  the  course  of  valvular  lesions  as  well,  as 
Mackenzie  has  proved.  The  case  cited  on  page  350  gives  an  example  of  such  an  irregularity 
arising  during  such  an  attack  and  subsiding  a  few  days  later  after  rest  and  digitalis.  Five 
days  later  the  rhythm  became  regular  and  the  auricles  were  contracting  once  more.  When 
the  overstrain  is  more  protracted  the  auricular  contraction  may  remain  absent  for  weeks 
and  even  months,  and  most  frequently,  if  it  has  persisted  for  a  considerable  length  of  time, 
permanent  changes  set  in  in  the  musculature  of  the  sinus  region  (Keith,  Schonberg),  and 
regularity  is  never  regained.  The  pulse  has  become  permanently  irregular  (pulsus  irregu- 
laris perpetuus,  arrhythmia  perpetua).     As   has   been  seen  on    page  77,  the  arrhythmia 


BROKEN   CARDIAC   COMPENSATION.  141 

itself  slows  the  blood  stream  and  the  diseased  condition  of  the  sinus  prevents  the  heart 
from  compensating  for  this  by  a  greater  number  of  contractions.  The  velocity  of  the 
circulation  is  thus  self-limited.  Only  a  certain  amoimt  of  CO,  per  minute  can  be  taken  care 
of  and  any  excess  brings  on  overstrain. 

Changes  in  Venous  Pressure. —  Changes  in  pressure  in  the  systemic 
veins,  which  show  how  well  the  right  ventricle  is  pumping,  often  afford 
an  excellent  index  of  the  break  in  systemic  compensation,  rising  from 
normal  pressure  of  5-10  cm.  HjO  to  a  height  of  20  or  25  cm.  It  usually 
rises  when  the  patient's  condition  becomes  worse  and  falls  as  improvement 
sets  in  (Hooker  and  Eyster). 

The  arterial  pressure,  on  the  other  hand,  is  affected  by  too  many 
factors  to  show  characteristic  changes.  It  may  be  kept  up  until  shortly 
before  death,  by  asphyxia  of  the  medullary  centres  and  resultant  vaso- 
constrictor and  augmentor  stimulation;  or,  on  the  other  hand,  when  this 
mechanism  is  not  brought  into  play,  the  arterial  pressure  may  be  low  and 
the  pulse  may  be  small  and  weak. 

CARDIAC    FAILURE    WITH    A    SMALL    HEART. 

There  is  another  form  of  failure  of  the  circulation  which  sometimes 
occurs  as  the  result  of  exertion,  even  in  trained  athletes.  This  form  is 
accompanied  by  pallor,  a  small  rapid  pulse,  and  sometimes  even  by  syncope. 
However,  as  Dietlen  and  Moritz  have  shown,  it  is  not  accompanied  by  a 
dilatation  of  the  heart,  but,  on  the  contrary,  the  latter  is  smaller  than 
normally.  It  is  a  failure  of  the  rest  of  the  circulation  rather  than  of  the 
heart. 

It  must  be  admitted  that  this  condition  has  not  attracted  much  attention,  and  but 
little  can  be  said  of  the  mechanisms  involved.  The  pallor,  small  pulse,  and  small  heart, 
however,  are  features  which  are  also  common  to  the  condition  of  shock  and  the  cardiac 
neuroses.  In  these  conditions,  the  important  mechanical  factors  are  the  accumulation  of 
blood  in  the  dilated  abdominal  veins,  giving  rise  to  a  low  venous  pressure,  the  diminished 
filling  of  the  heart,  and  consequently  the  diminished  output  into  the  aorta.  The  symp- 
toms are  symptoms  of  "arterial  anaemia." 

The  causal  factor  in  bringing  about  this  condition  may  be  dilatation  of  the  veins. 
In  the  case  of  exercise  this  veno-  and  vasodilatation  may  result  either  reflexly  from  dis- 
turbed digestion,  or,  perhaps,  as  Henderson  suggests  for  somewhat  similar  conditions,  it  may 
set  in  when  the  rapidity  of  breathing  exceeds  that  necessary  to  aerate  the  blood,  even  to 
meet  the  increased  needs  of  the  body.  Under  these  conditions  CO2  leaves  the  lungs,  and 
hence  also  the  blood,  a  little  too  rapidly,  acapnia  results,  and,  as  its  first  effect,  allows  the 
veins  to  dilate  (see  page  31).  The  blood  thus  stagnates  in  the  veins.  As  a  matter  of  fact, 
Kraus,  Zuntz  and  Schumburg,  and  also  A.  Loewy  have  shown  that  at  this  stage  of  exercise 
lessCOj  is  given  off  from  the  lungs  than  before,  and  the  respiratory  quotient  CO.,  is  lessened. 
They  believe  that  oxidation  is  less  at  this  stage  and  hence  less  CO2  is  present  in  the  blood. 
In  other  words,  from  a  totally  different  stand-point,  and  years  before  Henderson's  experi- 
ment, it  was  rendered  probable  that  a  state  of  acapnia  is  present  at  the  stage  of  fatigue 
in  exercises  of  endurance,  and  therefore  that  the  mechanism  which  he  observed  to  be  active 
in  acapnia  is  largely  responsible  for  this  form  of  circulatory  failure. 

FUNCTIONAL   TESTS   OF   CARDIAC   EFFICIENCY. 

It  is  evident  from  the  facts  discussed  above  that  the  most  important 
question  in  the  functional  study  of  heart  failure  is  to  determine  accurately  the 
border-line  between  fatigue  and  overstrain,  to  distinguish  between  the  nor- 
mal and  the  pathological.     Various  tests  have  been  devised  for  this  purpose. 


142  DISEASES   OF   THE   HEART   AND    AORTA. 

1.  Postural  Change  in  Pulse=rate. — The  rise  in  the  pulse-rate  which  oc- 
curs when  the  patient  stands  after  lying  down  is  of  some  importance.  Under 
normal  conditions  the  acceleration  is  not  more  than  twenty  beats  per  minute,  the  average 
acceleration  for  normal  individuals  being  seven.  However,  this  depends  upon  many 
factors,  one  of  which  is  the  length  of  time  during  which  the  patient  has  lain  down,  his  state 
of  mental  excitement  or  quiet,  etc.  The  psychic  element  plays  a  particularly  important 
role  in  this  test. 

2.  Contraction  of  Antagonistic  Muscles.  —  Herz  has  introduced  another  procedure, 
the  self-checking  or  self-antagonizing  test  (Selbsthemmungsprobe).  He 
counts  the  pulse  over  a  period  long  enough  to  assure  a  reasonably  constant  rate  per  minute. 
The  patient  is  then  made  to  sit  down  and  very  slowly  flex  and  extend  the  right  forearm, 
putting,  all  the  while,  his  full  attention  upon  the  movement,  but  contracting  simultaneously 
the  flexor  and  extensor  muscles  of  the  arm,  and  attempting  to  antagonize  his  own  move- 
ment with  as  much  force  as  possible.  This  converts  the  exercise  into  a  mild  exercise  of 
strain.  Herz  states  that  in  normal  individuals  this  causes  no  change  in  pulse- rate, 
while  in  those  with  feeble  hearts  the  pulse-rate  is  slowed  5-20  beats  per  minute.  (Per- 
haps this  is  due  to  the  more  vigorous  expiratory  effort  which  accompanies  this  procedure 
in  persons  with  diseased  hearts.)  Cabot  and  Bruce  have  repeated  Herz's  observations, 
and  find  that  they  are  correct  in  at  least  a  certain  number  of  cases,  but  they  are  unwilling 
to  subscribe  to  his  general  rule.  The  writer  also  has  found  a  number  of  perfectly  strong 
and  healthy  individuals  who  give  Herz's  pathological  reaction. 

3.  Rise  of  Blood-pressure  on  Constricting  the  Femoral  Arteries.  —  Marey  (1881) 
demonstrated  that  in  normal  individuals  the  blood-pressure  rose  when  both 
femoral  and  both  brachial  arteries  were  compressed.  Katzenstein  found  that  on  com- 
pressing both  femoral  arteries  alone,  in 

Blood-pressure  Pulse-rate 

Normal  individuals Rose    5-15  mm Fell. 

Compensated  cardiac  lesions Rose  15-40  mm Unchanged  or  fell. 

Slight  cardiac  insufficiency Unchanged Unchanged  or  rose. 

Very  weak  hearts Fell Fell. 

Hoke  and  Mende  and  others  have  repeated  Katzenstein's  observations,  and  find  that, 
though  these  results  hold  true  in  general,  the  method  is  unreliable  as  a  test  and  in  bad 
cases  is  too  dangerous  for  use. 

4.  Rise  of  Blood'pressure  upon  Exercise. — Another  method,  introduced  by  Graupner, 
of  Nauheim,  depends  upon  the  rise  of  blood-pressure  which  occurs  dur- 
ing exercise.  Graupner  found  that,  as  Masing  had  shown,  mild  rapid  exercise,  such 
as  walking  up  and  down  stairs  rapidly,  etc.,  caused  a  rise  of  blood-pressure  in  normal  indi- 
viduals but  a  fall  of  pressure  in  those  with  failing  hearts.  His  observations  have  been 
repeated  on  a  considerable  series  of  patients  by  Baur  (also  of  Nauheim).  Baur  used  the 
stationary  bicycle  as  a  test,  regulating  the  effort  by  applying  a  loaded  brake  to  the  wheels. 
He  found  that  in  normal  individuals  there  was  at  first  a  rise  of  5-10  mm.  Hg  and  later  a 
fall  of  5-10  mm.,  while  in  insufficient  hearts  there  was  a  fall  of  5-20  mm.  Hg.  The  hmit 
of  performance  of  the  latter  was  45-300  Hg  of  work,  however,  only  a  small  fraction  of  that 
which  could  be  done  by  the  normal  individuals.  Cabot  and  Bruce  also  have  repeated  and 
confirmed  Graupner's  observation,  and  believe  that  it  will  prove  of  assistance  as  an  aid  in 
functional  diagnosis. 

That  a  close  relationship  exists  between  the  increase  in  blood-pressure 
and  the  increase  in  tonicity  (stimulation  of  augmentor  fibres),  which  results 
from  strain  put  upon  the  heart,  may  be  seen  from  the  curves  of  Hirsch- 
felder  and  Cameron  in  the  dog's  heart  (quoted  on  page  135,  and  shown  in 
Figs.  118  and  119).  It  is  probable  that,  in  most  cases,  rise  of  pressure  cor- 
responds to  increased  systolic  output  and  concomitant  increase  in  tonicity. 
It  must  be  realized,  however,  that  in  some  cases  the  rise  may  be  second- 
ary to  stimulation  of  the  vasoconstrictor  centre  from  medullary  stasis  or 
asphyxia,  but  may  represent  an  unfavorable  condition. 


FUNCTIONAL  TESTS  OF  CARDIAC  EFFICIENCY.  143 

Several  objections  may  be  made  to  the  value  of  this  test: 

1.  G.  A.  Gordon  in  G.  A.  Gibson's  clinic  and  also  Professor  Dawson,  in  collaboration 
with  Professor  Eyster  and  also  with  Mr.  Hetfield,  have  shown  that  the  blood-pressure 
in  trained  athletes  falls  during  mild  exercise  exactly  as  it  does  in  broken 
compensation  ;  also  that  it  falls  when  the  "second  wind"  is  acquired  and  while  the 
person's  functional  power  is  increasing  rather  than  decreasing. 

2.  As  already  shown  by  Masing,  the  greatest  rises  of  blood-pressure 
occur  in  old  and  feeble  persons,  whom  the  exercise  brings  near  to  the  border-line  of  cardiac 
overstrain. 

3.  In  persons  in  whom  the  fall  in  blood-pressure  occurs  as  a  result  of  the  test  exercise, 
the  general  symptoms,  respiratory  distress,  cyanosis,  etc.,  to  say  nothing  of  the  diminished 
decrease  in  the  size  of  the  pulse,  tachycardia  and  arrhythmia  resulting,  are  more  than  suf- 
ficient evidence  that  the  patient's  strength  has  been  overtaxed. 

4.  These  simpler  clinical  manifestations  are  more  delicate  indices  and  are  less  ambig- 
uous signs  than  are  the  changes  in  blood-pressure. 

The  recent  studies  of  Schott,  de  la  Camp,  v.  Criegern,  Hornung,  Moritz  and  his  pupils, 
taken  in  conjunction  with  the  physiological  experiments  of 
Frank,  Hi rschf elder ,  and  Cameron,  indicate  that  the  only  true 
numerical  criterion  of  cardiac  efficiency  is  whether  a  given 
strain  causes  it  to  diminish  in  size  (increase  in  to  nicity=  stimu- 
lation)   or  to   dilate    (decrease    in   t onicity  =  overstrain). 

Functional  studies  upon  the  border-land  between  functional  suffici- 
ency and  cardiac  failure  are  of  the  most  fundamental  importance,  and  all 
the  facts  added  to  our  knowledge  of  the  subject  are  of  the  greatest  value 
in  adding  to  our  understanding  of  the  subject. 

Observation  versus  Estimation. — However,  it  must  be  admitted  that, 
in  order  to  be  decisive,  all  these  tests  usually  have  to  be  pushed  to  a  point 
at  which  the  appearance,  sensations,  and  signs  of  the  patient  are  in  them- 
selves perfectly  characteristic  of  cardiac  insufficiency,  and  at  which,  for 
diagnostic  purposes,  a  little  common-sense  observation  is  at  least  as  unam- 
biguous as  observation  with  elaborate  apparatus.  This  does  not  mean 
that  exercise  tests  are  unimportant.  On  the  contrary,  they  are  of  the 
greatest  value;  and  no  change  in  the  patient's  mode  of  living  during  con- 
valescence or  during  after  life  should  be  undertaken  without  them.  But  their 
importance  depends  more  upon  the  care  with  which  the  physician  watches 
the  general  appearance  and  condition  of  the  patient,  the  rapidity  with  which 
he  recovers  from  the  exercise,  his  general  condition,  and  whether  nervous- 
ness, irritability,  cough,  or  insomnia  have  set  in  during  the  twenty-four 
hours  following  it,  than  in  the  numerical  changes  which  occur  at  the  moment 
of  exercise.  The  symptoms  to  be  looked  for  as  evidence  of  overwork  are 
discussed  in  more  detail  in  the  instructions  for  giving  Schott  exercises  (page 
195).  These  are  subtler  manifestations  resulting  from  smaller  changes 
than  may  be  detected  by  even  the  most  refined  observations  by  mechan- 
ical methods,  and  which  are  less  easily  masked  by  ambiguities.  Moreover, 
it  must  be  realized  that  any  one  form  of  exercise  furnishes  data  which 
may  depend  as  much  upon  the  condition  of  the  skeletal  muscles  as  upon 
the  heart.  The  blacksmith  with  a  diseased  heart  may  be  able  to  do  more 
work  than  the  book-keeper  with  neurasthenia,  and  yet  under  the  conditions 
in  which  he  lives,  even  if  not  under  the  strength  test  arranged  for  the  average 
man,  the  blacksmith's  heart  may  be  failing. 

Relation  of  Functional  Test  to  Mode  of  Life. — In  diagnosis,  prognosis, 
and  therapy,  the  testing  of  functional  insufficiency  is  a  matter  of  sociology 


144  DISEASES   OF   THE   HEART   AND    AORTA. 

as  well  as  physiology.  The  important  question  is  not  what  the 
patient  can  do  in  a  gymnasium,  but  what  he  can  do  and 
what  he  can  not  do  in  every-day  life.  Each  man  must  be  fit 
for  his  own  mode  of  life  or  must  be  made  to  change-it.  His  cardiac  power 
must  be  studied  with  reference  to  that  mode  of  life  rather  than  with  ref- 
erence to  a  rigid  scheme. 

Probably  the  most  thorough  system  of  routine  functional  testing  ever 
instituted  was  that  resorted  to  by  J.  M.  da  Costa  during  the  Civil  War  before 
he  permitted  his  convalescents  from  cardiac  overstrain  to  return  to  active 
duty  with  their  regiments.  He  subjected  them  first  to  light  camp  duties, 
then  to  guard  duty,  then  to  provost  duty,  and  later  made  them  run  frequent 
races  comparable  to  charges  upon  a  battlefield — each  test  commensurate 
with  the  mode  of  life  which  the  patient  was  about  to  live.  Step  by  step 
he  ascertained  the  endurance  of  his  patients  without  overstraining  them, 
and  thus  obtained  a  series  of  permanent  cures  which  stands  as  a  worthy 
monument  to  one  of  the  most  careful  and  brilliant  of  American  clinicians. 


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to  the  Maximum  Volume  of  Blood  sent  out  by  the  Left  Ventricle  in  a  Single  Beat  and 
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the  Work  done  by  the  Heart,  Phil.  Tr.  Roy.  Soc,  Lond.,  1884,  Pt.  i,  139. 

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1888,  ii,  1321.  Contributions  to  the  Physiology  and  Pathology  of  the  Mammalian 
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Hirschfelder,  A.  D.:  Recent  Studies  on  the  Circulation  and  their  Importance  to  the  Prac- 
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of  the  Heart,  Am.  J.  Physiol.,  Bost.,  1898,  i,  215. 

Meylan,  G.  L.:  Harvard  University  Oarsmen,  Harvard  Grad.  Mag.,  1904,  xii,  362,  543. 

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1878,  Ixxii,  375. 

Sahli,  H.:  Zur  Pathologie  des  Lungenoedems,  Ztschr.  f.  klin.  Med.,  Berl.,  1888,  xiii,  482. 
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10 


146  DISEASES   OF   THE   HEART   AND    AORTA. 

Lungenoedem,  p.  7  (also  Ztschr.  f.  klin.  Med.,  Leipz.,  1887,  xii,  550).  V.  Basch,  S.: 
Ueber  eine  Function  des  Capillardrucks  in  den  Lungenalveolen,  p.  49;  Pathologie 
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Lehre  vom  acuten  allgemeinen  Lungenoedem,  p.  80  (also  Ztschr.  f.  klin.  Med., 
xvi).  Bettelheim,  K.,  and  Kauders,  F.:  Experimentelle  Untersuchungen  ueber  die 
kiinstlich  erzeugte  Mitralinsufficienz  und  ihren  Einfluss  auf  Kreislauf  und  Lunge, 
p.  144.  V.  Basch,  S.:  Ueber  Lungenschwellung  und  Lungenstarrheit,  p.  171;  Zur 
Lehre  von  der  cardialen  Dyspnoe,  p.  183;  Ueber  Lungenschwellung  bei  der  cardialen 
Dyspnoe  des  Menschen,  p.  198.  Kauders,  F.:  Ueber  einige  Experimente  zur  Lehre 
von  der  Cardialen  Dyspnoe,  p.  211.  Vol.  ii.  Zemer,  Th.  J.:  Ueber  den  Einfluss  der 
Digitalis  auf  die  Respiration,  p.  19.  Grossmann,  M.:  Ueber  Stauungshyperaemie  in 
den  Lungen,  p.  30.  Kornfeld,  S.:  Experimenteller  Beitrag  zur  Lehre  vom  Venen- 
druck  bei  Fehlern  des  linken  Herzens,  p.  126.  Vol.  iii.  Hegglin,  C:  Experimentelle 
Untersuchungen  ueber  die  Wirkung  der  Douche,  p.  1.  Zemer,  Th.  J.:  Khnisch- 
experimentelle  Untersuchimgen  ueber  die  cardiale  Dyspnoe,  p.  77.  Buday,  K.: 
Ueber  die  HerzfuUung  wahrend  des  Lebens  und  nach  dem  Tode,  p.  106.  Winkler,  F.: 
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makol.,  Leipz.,  1901,  xlv,  186. 

MacCallum,  W.  G.,  and  McClure,  R.  D.:  On  the  Mechanical  Effects  of  Mitral  Stenosis  and 
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Bull.,  1906,  xvii. 

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Physiol.,  Bonn,  1900,  Ixxxii,  1. 

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1897,  Heft  3. 

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Herz,  M.:  Eine  Funktionspriifung  des  Kranken  Herzens,  Deutsch  med.  Wchnschr., 
Leipz.,   1905,  xxxi,  215. 

Cabot,  R.  C,  and  Bruce,  R.  B.:  The  Estimation  of  the  Functional  Power  of  the  Cardio- 
vascular Apparatus,  Am.  J.  M.  Sc,  Phila.  and  N.  York,  1907,  cxxxiv,  491. 

Marey,  E.  J.:  La  circulation  du  sang  a  I'^tat  physiologique  et  dans  les  maladies,  Paris,  1881. 

Katzenstein:  Ueber  eine  neue  Funktions  priifung  des  Herzens,  Deutsche  med.  Wchnschr., 
Leipz.  and  Berl.,  1905,  xxxi,  695. 

Hoke,  E.,  and  Mende,  J.:  Ueber  die  Katzensteinsche  Methode  zur  Priifung  der  Herz- 
kraft,  Beri.  klin.  Wchnschr.,  1907,  xliv,  .304. 

Levy:  Ueber  Kraftmessung  des  Herzens,  Ztschr.  f.  khn.  Med.,  Berl.,  1906,  Ix,  74. 

Fellner,  B.,  and  Riidinger,  C:  Beitrag  zur  Funktionspriifung  des  Herzens,  Berl.  klin. 
Wchnschr.,  1907,  xliv,  417,  475. 

Graupner:  Die  Messung  der  Herzkraft,  Miinchen,  1905. 

Baur,  Fr.:  Zur  Bestimmung  der  Leistungsfahigkeit  des  gesunden  und  kranken  Herzens 
durch  Muskelarbeit,  Verhandl.  d.  Kong.  f.  inn.  Med.,  Wiesb.,  1904,  xxi,  620. 


III. 

SYMPTOMS  OF  CARDIAC  DISEASE. 

The  symptoms  for  which  a  patient  suffering  from  cardiac  disturbance 
presents  himself  to  the  physician  are  variable,  and  frequently  seem  so  far 
removed  from  the  site  of  disease  as  to  mask  their  real  origin  and  even  to  lead 
to  mistakes  in  diagnosis.  Accordingly,  it  is  important  to  consider  the 
symptoms  early  and  the  conditions  giving  rise  to  them,  remembering  that 
in  general  they  are  due  to  (1)  slowing  of  the  circulation  and  local  anaemia 
or  accumulation  of  COj;  (2)  overfilling  of  the  veins  with  blood;  (3)  disturb- 
ances in  the  nervous  system,  of  circulatory  origin. 

The  following  are  the  main  symptoms  associated  with  cardiac  diseases: 
(1)  shortness  of  breath;  (2)  cough;  (3)  swelling  of  the  feet  and  legs; 
(4)  urinary  disturbances;  (5)  palpitation  of  the  heart,  precordial  pain, 
pain  down  the  arms;  (6)  digestive  disturbances,  indigestion,  vomiting, 
abdominal  pain,  jaundice;  (7)  general  nervousness,  occasionally  transitory 
delusions  and  hallucinations,  sometimes  fainting  spells. 

All  these  symptoms  are  liable  to  be  increased  after  exercise, 
excitement,  or  worry,  on  account  of  the  increased  heart-rate  and 
often  increased  blood-pressure  that  accompany  them,  and  the  conse- 
quent increase  in  the  work  of  the  heart.  They  are  also  much  increased 
by  damp  and  sultry  weather  when  there  is  little  air  stirring.  The  patient's 
color  is  then  usually  pale,  showing  a  vasoconstriction  to  which  some  of  the 
embarrassment  is  probably  ascribable.  The  symptoms  usually  improve 
when  the  weather  becomes  clear. 

RESPIRATORY   DISTURBANCES. 
DYSPNCEA. 

Shortness  of  breath  is  usually  the  earliest  and  most  common  sign  of 
cardiac  failure  and  especially  of  failure  of  the  left  ventricle  (broken  com- 
pensation). The  foundation  for  this  doctrine  was  laid  by  the  classical 
experiments  of  Welch  under  Cohnheim's  direction.  Welch  demonstrated 
that  in  conditions  in  which  the  force  of  the  left  ventricle  was  impaired 
without  impairment  of  the  right,  oedema  and  congestion  of  the  lungs  set  in. 

V.  Basch  and  his  pupils,  Grossman,  Bettelheim,  and  Kauders,  have 
shown  —  in  a  very  careful  series  of  investigations  upon  animals — that 
dyspnoea  and  the  other  respiratory  disturbances  of  heart 
failure  are  due  chiefly  to  stasis  in  the  pulmonary  capil- 
laries and  veins,  and  are  associated  with  rise  of  pressure  in  the  left 
auricle.  Under  these  circumstances  the  elasticity  of  the  lungs  is  probably 
diminished  and  the  volume  of  lung  tissue  increases.  The  respiratory 
excursion  decreases.  These  conditions  disappear  when  the  output  of  the 
left  ventricle  (and  hence  the  suction-pump  action  of  that  chamber)  in- 

147 


148  DISEASES   OF   THE    HEART    AND    AORTA. 

creases  sufficiently  to  pump  out  the  excess  of  blood  from  the  lungs  and 
remove  the  stasis.  Accordingly,  as  is  the  common  clinical  experience, 
severe  dyspnoea  is  an  early  sign  of  mitral  lesions,  which  readily  comes 
and  goes  with  slight  overstrains;  while  in  aortic  disease  it  is  a  sign  of  a 
severe  break  in  compensation,  and  often  indeed  of  a  secondary  mitral 
insufficiency. 

This  group  of  symptoms  —  cough,  dyspnoea,  cardiac 
asthma,  pulmonary  oedema,  pulmonary  hemorrhage  — 
constitute  a  group  of  symptoms  characteristic  of  stasis 
in  the  pulmonary  veins  (broken  pulmonary  compensa- 
tion), just  as  cyanosis,  enlargement  of  the  liver,  and 
ascending  oedema  are  characteristic  of  failure  of  the 
right  heart.  In  Wilkinson  King's  "safety-valve  action  of  the  right 
ventricle"  failure  of  the  latter  substitutes  a  state  of  broken  systemic  com- 
pensation for  one  of  broken  pulmonary  compensation. 

Rubow  has  shown  by  spirometric  investigations  that  in  cardiac  dys- 
pnoea there  is  a  tendency  for  the  lungs  to  assume  the  greatest  possible  vol- 
ume (diaphragm  descends  lower  and  lower)  just  as  is  the  case  in  emphysema. 

According  to  Kraus  the  amount  of  Oj  taken  up  by  the  blood  and  of  CO^  given  off  per 
minute  is  practically  unchanged  in  cardiac  failure.  The  conditions  are  therefore  practically 
analogous  to  Zuntz  and  Schumburg's  experiment,  in  which  increasing  the  COj  in  the  inspired 
air  caused  polypnoea  and  caused  the  total  amount  of  air  taken  into  the  lungs  per  minute 
to  rise  tremendously  without  altering  the  amount  of  oxygen  taken  up  by  the  blood.  It 
is  probable  that  stasis  in  the  pulmonary  capillaries  stimulates  the  vagus,  endings  in  the 
same  way  as  does  COj. 

Orthopnoea. — One  of  the  most  striking  features  of  cardiac  dyspnoea  is 
the  fact  that  it  is  increased  in  the  reclining  posture  and  relieved  by  sitting 
up  (orthopnoea),  although  this  position  favors  the  accumulation  of 
oedema  in  the  legs,  and,  as  Erlanger  and  Hooker  have  shown,  impedes  the 
total  velocity  of  the  circulation.  For  this  fact  there  may  be  several  expla- 
nations, or,  more  accurately,  there  may  be  several  factors  involved: 

1.  As  Rubow  has  shown,  when  the  patient  is  propped  up,  his  liver  and  diaphragm 
descend,  and  there  is  thus  more  air  space  available  in  the  thoracic  cavity. 

2.  Since  the  head  up  and  feet  down  position  tends  to  impede  the  return  of  venous 
blood  from  the  lower  extremities,  trunk,  and  abdomen,  it  thus  tends  to  equalize  the  activi- 
ties of  the  right  and  left  ventricles.  By  slowing  the  inflow  of  blood  into  the  lungs  it  enables 
the  weakened  left  ventricle  to  deplete  the  pulmonary  capillaries  more  effectually  than 
would  occur  if  more  blood  were  throwTi  into  them  by  the  relatively  stronger  right  ventricle. 

3.  In  the  head  up  position  the  veins  of  the  medulla  drain  more  readily,  thus  diminish- 
ing venous  stasis  in  the  medulla  and  consequently  also  diminishing  the  effect  of  direct  COj 
stimulation  of  the  vagus  and  respiratory  centres.  This  effect  of  the  erect  position  in  dimin- 
ishing the  volume  of  (i.e.  the  blood  in)  the  brain  is  well  known  to  brain  surgeons,  who  some- 
times make  use  of  it  for  penetrating  to  otherwise  inaccessible  places. 

Cardiac  dyspnoea  is  particularly  marked  during  sleep,  partly  because 
the  diminished  sensitiveness  of  the  respiratory  centres  allows  COj  to  accu- 
mulate (if  only  momentarily)  with  greater  ease  than  during  periods  of  wake- 
fulness, and  partly  because  the  muscles  of  the  larynx  relax,  the  laryngeal 
slit  is  narrowed,  and  air  enters  the  lungs  with  more  difficulty,  thus  allow- 
ing a  slight  asphyxia  to  set  in. 

Cardiac  Asthma. — Occasionally  the  respiratory^  distress  takes  the  form 
of  a  definite  paroxysmal  dyspnoea  or  cardiac  asthma.     These  paroxysms 


SYMPTOMS   OF   CARDIAC   DISEASE.        .  149 

are  particularly  common  in  aortic  insufficiency  or  coronary  sclerosis.  They 
frequently  occur  at  the  moment  of  awakening;  or,  more  accurately,  the 
patient  is  awakened  by  the  need  of  air,  CO2  having  accumulated  during 
sleep,  owing  partly  to  the  slower  respiration,  partly  to  the  above-men- 
tioned relaxation  of  the  laryngeal  muscles.  This  factor  may  also  give  rise 
to  an  acute  failure  of  the  left  ventricle  from  impaired  cardiac  tonus  which 
arises  during  the  mild  asphyxia  that  has  preceded.  Perhaps  the  dyspnoea 
is  due  partly  to  heart  failure  and  partly  to  respiratory  failure. 

While  the  patient  is  awake,,  such  attacks  are  sometimes  brought  on 
by  the  act  of  defecation.  This  is  not  surprising,  since  defecation  presents 
a  typical  Valsalva's  experiment,  in  which,  as  previously  shown,  a  great 
strain  is  thrown  upon  the  left  ventricle,  sometimes  severe  enough  to  pro- 
duce a  functional  mitral  insufficiency. 

Morphine  and  Strychnine  in  Cardiac  Dyspnoea. — Such  attacks  of  car- 
diac asthma  may  be  relieved  by  morphine,'  but  the  continued  use  of 
morphine  for  this  purpose  often  has  a  bad  effect.  Though  it  momenta- 
rily relieves  the  distress,  it  also  diminishes  the  irritability  of  the  respira- 
tory centre  and  thus  allows  still  more  CO2  to  collect  in  the  blood.  The 
patient  then  requires  still  more  morphine  to  quiet  him,  and  a  vicious 
circle  is  introduced: 

Accumulation  of  CO  3         ^^  r  j 

in  the  lungs  "^   Paroxysm  of  dyspncBa 

t        /  1 

Diminished  irritability         ,,      ,  . 

,  .     ,  .         <—  Morphine 

of  respiratory  centre  ^ 

On  the  other  hand,  the  patient  so  quickly  acquires  the  morphine 
habit  that  frequently  he  brings  on  a  paroxysm  of  dyspnoea  voluntarily  in 
order  to  get  the  drug,  and  does  himself  considerable  harm  by  this  effort. 

Under  these  conditions  strychnine  is  the  drug  indicated  by  its  pharma- 
cological action  in  stimulating  the  respiratory  centre  (as  Eyster  has  shown) . 
Where  strychnine  (.002  to  .005  Gm,  =  gr.  -^j^  to  gr.  J^)  or  with  atropine 
(.0005  Gm.  to  .001  Gm.  =  gr.  y^^^  to  gr.  -gV)  does  not  suffice,  morphine  may 
have  to  be  given,  but  it  is  best  to  give  some  strychnine  along  with  it.  After 
the  first  dose  it  is  frequently  possible  to  obtain  the  quieting  psychic  effect 
by  injections  of  distilled  water  or  of  strychnine  alone  without  giving  rise 
to  the  morphine   habit. 

Cardiac  Asthma  from  Nasal  Disease. — Another  form  of  asthma  with  cardiac  symptoms 
has  its  origin  not  within  the  heart  but  in  the  nose.  Frangois-Franck  in  1889  was  able  to 
demonstrate  that  cough,  laryngeal  spasm  (false  croup),  asthma,  and  a  reflex  bronchitis 
arise  reflexly  from  stimulation  of  the  nasal  mucosa.  He  was  able  to  reproduce  these  phe- 
nomena in  animals  by  stimulating  the  mucosa  of  the  septum.  They  were  accompanied 
by  acceleration  of  the  heart  and  vasoconstriction.  They  did  not  appear  when  the  latter 
had  been  cocainized;  or  if  they  had  once  set  in,  they  disappeared  on  cocainization.  He 
found  that  these  effects  were  much  more  pronounced  in  animals  with  experimental  aortic 
insufficiency  than  in  normal  animals,  and  he  believes  that  such  exaggerated  responses  to 
nasal  reflexes  are  responsible  for  many  of  the  paroxysmal  respiratory  disturbances  in  car- 
diac patients  suffering  from  cardiac  disease,  and  especially  from  aortic  insufficiency.  It 
is  possible  that  they  may  give  rise  to  some  of  the  vasomotor  crises. 

It  is  important  to  differentiate  cardiac  asthma  from  the  bronchial  form. 
Both  may  be  accompanied  by  bronchitis  and  by  the  presence  of  rales. 
In  the  cardiac  form  there  is  no  impediment  to  either  expiration  or  inspira- 


150  DISEASES   OF   THE    HEART    AND    AORTA. 

tion,  and  hence  only  a  simple  polypncea  is  observed,  while  in  bronchial 
asthma  there  is  stenosis  of  the  smaller  bronchi  with  hinderance  to  both 
expiration  and  inspiration,  and  hence  a  peculiar  labored  and  wheezing 
breathing  with  prolongation  of  expiration  which  is  quite  characteristic. 

C.  M.  Cooper  (The  Respiratory  Ratio:  A  Preliminary  Note,  J.  Am.  M.  Asso.,  Chicago, 
1909,  lii,  1182),  suggests  that  the  differential  diagnosis  in  doubtful  cases  may  sometimes 
be  made  by  noting  the  ratio  between  the  periods  during  which  the  breath  can  be  held  in 
full  inspiration  and  those  in  which  it  may  be  held  in  full  expiration.  In  normal  individ- 
uals the  breath  maybe  held  in  inspiration  from  40  to  70  seconds;  in  expiration  from  20  to 

35  seconds  (  i.e.,  ratio  _     „     ).     In  patients  with  cardiac  insufficiency  this  ratio  is  pre- 

served,  though  the  periods  are  shortened  (  tt/-     ^^  bronchial  asthma,  on  the  other 

hand,  the    breath  can   be  held  longer  in  expiration  than  in  inspiration  and  the  ratio 

is   reversed   (^). 

It  seems  probable  that  this  ratio  will  prove  of  great  value  in  differentiating  be- 
tween asthmatic  attacks  due  to  acute  failure  of  the  left  ventricle  and  those  which  arise 
in  cases  of  cardiac  diseases,  from  reflexes  of  nasal  or  visceral  origin. 

PULMONARY    CEDEMA. 

Occasionally  the  attack  of  cardiac  failure  is  very  severe  and  is  accom- 
panied by  oedema  of  the  lungs.  The  above-mentioned  experiments  of 
Welch  and  Cohnheim,  and  later  of  v.  Basch  and  his  pupils,  have  shown 
that  this  is  due  to  pulmonary  stasis  from  acute  failure  of  the  left  ventricle. 
It  is  most  frequent  in  cases  of  mitral  stenosis  in  which  pulmonary  stasis 
readily  sets  in,  and  is  the  complication  particularly  to  be  feared  during 
pregnancy  and  labor. 

Experimentally,  pulmonary  oedema  is  readily  produced  by  overstraining  the  left 
ventricle  through  an  overdose  of  adrenalin  (L.  Loeb')-  Besides  conditions  of  cardiac 
disease  it  is  occasionally  encountered  after  operations  in  which  adrenalin  has  been  used, 
especially  when  in  large  amounts  or  upon  surfaces  from  which  it  is  readily  absorbed.  Oc- 
casionally, as  in  a  case  recently  known  to  the  writer,  sudden  death  results  from  this  cause 
from  an  operation  otherwise  trivial. 

J.  J.  Miller  and  S.  A.  Matthews  have  recently  investigated  the  action  of  numerous 
poisons  in  producing  pulmonary  oedema,  and  have  found  that  mechanical  factors  in  the 
circulation  (failure  of  the  left  ventricle)  are  the  immediate  cause  of  the  pulmonarj'  oedema 
after  adrenahn,  iodides,  and  iodine,  but  that  acetic  ether,  nitric  oxide,  and  ammonia  cause 
it  to  app)ear  without  any  evidence  of  disproportion  between  the  action  of  the  two  ven- 
tricles. These  substances  apparently  act  entirely  by  injuring  the  walls  of  the  pulmonary 
vessels  and  by  increasing  the  secretion  of  the  alveolar  walls,  cells,  and  pulmonary  lymph. 

Signs  of  Pulmonary  (Edema.  —  The  onset  of  pulmonar}^  oedema  is 
marked  by  pallor,  cyanosis,  cough,  coarse  moist  rales  throughout  the  chest, 
and  often  by  a  frothy  serous  expectoration  which  may  be  very  profuse. 
Friedrich  Miiller  has  shown-  that  this  expectoration  contains  considerable 


'  Haven  Emerson  has  shown  that  this  occurs  only  when  the  chest  is  closed,  not  when 
the  chest  is  opened  and  artificial  respiration  substituted,  and  that  it  can  often  be  cured 
by  artificial  respiration  with  bellows  inflation.  Barringer  reports  good  results  from  artificial 
respiration  in  one  patient. 

'  To  demonstrate  the  presence  of  albumen  add  dilute  acetic  acid  to  the  sputum  to 
precipitate  all  the  mucin,  filter,  and  then  precipitate  the  albumen  from  the  filtrate  by  the 
addition  of  potassium  ferrocyanide. 


SYMPTOMS   OF   CARDIAC   DISEASE.  151 

albumen,  a  fact  of  great  diagnostic  importance  in  doubtful  cases.  These 
symptoms  constitute  a  signal  for  immediate  action. 

Treatment. — The  strain  upon  the  left  ventricle  may  be  relieved  by 
inhalations  of  amyl  nitrite,  and  its  strength  may  be  increased  within  a  few 
minutes  by  intravenous  injection  of  strophanthus.  The  most  certain  pro- 
cedure, however,  is  venesection,  since  it  diminishes  the  work  of  the 
right  heart  at  once  and  thus  enables  the  left  ventricle  to  equalize  conditions. 
Accordingly  pulmonary  oedema  is  the  signal  for  venesection  in  any  except 
the  most  anaemic  persons. 

For  the  oedema  itself  atropine  (0.5-1.0  mg.,  y^^  to  -gV  gr.  hypodermati- 
cally)  should  be  given,  inasmuch  as  it  diminishes  the  bronchial  secretions 
and  thus  does  away  with  the  oedema.  In  desperate  cases  larger  doses 
should  be  used. 

HEMORRHAGE    FROM    THE    LUNGS. 

As  a  result  of  engorgement  of  the  pulmonary  capillaries  or  of  per- 
manent injury  to  their  walls,  hemorrhages  from  the  lungs  may  occur  in 
any  acute  cardiac  overstrain,  ,but  they  are  most  frequently  seen  in  cases 
of  mitral  disease.  In  itself  such  a  pulmonary  hemorrhage  is  of  no  impor- 
tance, although  by  relieving  the  congestion  it  may  bring  a  great  deal  of 
subjective  relief  to  the  patient.  On  the  other  hand,  the  conditions  which 
bring  them  on  acutely  are  frequently  those  of  severe  overstrain.  They 
are  particularly  common  in  mitral  disease,  in  pulmonary  insufficiency 
and  sclerosis,  and  congenital  heart  diseases. 

It  is  always  of  the  greatest  importance  to  differentiate  between  such  an  hemoptysis 
and  that  of  an  early  pulmonary  tuberculosis,  and  only  the  most  careful  repeated  examina- 
tions, coupled  with  the  presence  of  the  cardiac  lesion  and  the  absence  of  signs  of  pulmonary 
disease,  give  sufficient  grounds  to  exclude  the  latter.  It  is  particularly  important  to  exam- 
ine for  tubercle  bacilli  in  the  blood  spit  up,  since  after  a  hemorrhage  they  may  not  be  pres- 
ent again  in  the  sputum  for  several  months. 

Rest  and  the  general  measures  which  diminish  pulmonary  engorgement 
constitute  the  treatment. 

PULMONARY  EMBOLISM  AND  HEMORRHAGES. 

Pulmonary  embolism  with  infarction  is  a  not  uncommon  complica- 
tion when  a  clot  forming  in  the  right  auricle  or  ventricle  is  loosened  into 
the  circulation  and  lodges  in  some  branch  of  the  pulmonary  artery.  These 
infarcts  may  be  large  or  small,  dependent  upon  the  artery  occluded,  and 
upon  their  size  .depends  the  severity  of  the  symptoms  and  the  onset  of 
dyspnoea. 

In  all  these  cases  there  is  an  area  of  dulness,  tubular  breathing, 
and  increased  vocal  fremitus  over  some  parts  of  the  lung,  and  the  expectoration  of  a  slimy, 
bloody  or  prune-juice  sputum,  which  differs  from  that  occurring  in  brown 
induration  in  being  much  richer,  deeper  in  color,  and  in  containing  a  great  deal  of  more  or 
less  changed  blood  intimately  mixed  with  the  mucus  instead  of  somewhat  separate  from  it. 
Pulmonary  embolism  is  sometimes  fatal  when  a  large  vessel  is  occluded,  but  usually  not 
so  in  the  first  instance.  Exactly  when  a  single  embolus  will  be  followed  by  a  shower  of 
emboli  and  a  fatal  result  cannot  be  foretold,  and  the  patient  lives  continually  under  a 
sword  of  Damocles,  although  in  some  cases  he  may  live  for  several  years  without  further 
disturbance. 


152 


DISEASES   OF   THE   HEART   AND   AORTA. 


CHEYNE-STOKES    BREATHING. 

Cheyne,  of  Dublin,  described  a  peculiar  form  of  respiration  in  which 
there  are  occasional  pauses  of  variable  duration,  from  several  seconds  to 
half  a  minute,  followed  by  inspirations  at  first  slow,  then  more  rapid,  then 
again  lapsing  into  a  pause.  It  was  again  described  by  Stokes  in  1846  and 
is  very  common  in  bad  cases.  This  phenomenon  is  particularly  frequent 
in  heart  cases,  especially  in  aortic  disease,  and  is  usually  seen  when  the 
patient  is  asleep.  It  is  also  common  in  cases  of  brain  tumor,  apoplexy,  or 
any  condition  where  there  is  an  increased  intracranial  tension.  Not  infre- 
quently, in  cardiac  disease,  the  patient  is  in  a  state  of  coma  or  semicoma 
during  the  periods  of  apnoea  but  fully  conscious  during  the  periods  of 
dyspnoea.  During  the  former  the  pupils  are  contracted  and  do  not  react; 
during  the  latter  they  widen  and  react  once  more. 


Fig.  122. —  The  two  types  of  Cheyne-Stokes  respiration  in  their  relations  to  the  blood -pressure 
curves.  (After  Eyster.)  A.  Intracranial  pressure  type — apncea  accompanies  slowing  of  the  pulse  and 
fall  of  blo<»d-pressure.  B.  The  cardiac  type — apncea  associated  with  rise  of  blood-pressure  and  quick- 
ening of  the  pulse-rate. 


Eyster  has  found  that  the  occurrence  of  Cheyne-Stokes  respiration  is  always  asso- 
ciated with  the  slow  periodic  changes  of  blood-pressure  known  as  Traube-Hering  waves. 
He  distinguishes  two  types:  In  the  first,  which  is  always  associated  with  increased  intra- 
cranial tension,  as  in  brain  tumor,  meningitis,  uraemia,  the  period  of  respir- 
atory activity  is  associated  with  a  rise  of  blood-pressure  and  quickening 
of  the  pulse,  the  period  of  apnoea  with  a  fall  of  blood-pressure  and  s  1  o w- 
ing  of  the  pulse  (Fig.  122,  A). 

In  the  second  type,  the  common  form  in  cardiac  and  arterial  disease,  the  respir- 
atory activity  is  associated  with  a  fall  in  blood-pressure  and  slowing  of 
the  pulse,  and  the  apnoea  is  associated  with  rise  in  blood-pressure  and  quick- 
ening  of  pulse-rate  (Fig.  122,  B).  Eyster  w^as  able  to  reproduce  the  first  group  in  animals 
by  raising  the  intracranial  tension,  and  found  that  whenever  the  intracranial  pressure 
was  above  the  mean  blood-pressure  apnoea  occurred.  Then  the  blood-pressure  rose  through 
asphyxial  stimulation  of  the  vasomotor  centre,  and  when  it  overtopped  the  intracranial 
pressure,  respirations  again  set  in.  The  converse  was  not  true  of  the  second  group  of 
cases,  and  neither  he  nor  any  other  observer  has  been  able  to  reproduce  this  more  com- 
mon tjrpe  or  analyze  its  causal  factors. 

Biot  has  described  another  type  of  respiration,  in  which  a  series  of  inspirations  equal 
in  rate  and  in  size  are  punctuated  by  long  apnoeic  pauses.  This  is  only  a  small  variety  of 
the  cases  showing  the  Cheyne-Stokes  type,  and  its  occurrence  and  causal  factors  seem 
to  be  about  the  same  as  the  latter. 

Mosso  has  also  depicted  another  group  of  periodic  respirations  occurring  at  high 
altitudes,  apparently  from  low  CO2  content  of  the  blood  reaching  the  vasomotor  centre 
(acapnia),  in  which  there  is  with  each  respiratory  group  rise  of  blood- 
pressure  and  slowing  of  the  pulse.  This  does  not  seem  to  occur  in  cardiac  or  intra- 
cranial cases. 


SYMPTOMS   OF   CARDIAC   DISEASE.  153 

Eyster  concludes  that  in  the  intracranial  pressure  type  the  Cheyne-Stokes  respiration 
is  due  to  the  fact  that  the  respiratory  centre  is  more  sensitive  to  aniemia  than  is  the  vaso- 
motor centre,  and  rapidly  loses  its  irritability,  regaining  it  when  circulation  is  reestablished. 

Therapeutically  Eyster  has  attempted  to  remedy  the  condition  by 
increasing  the  irritability  of  the  respiratory  centre,  (1)  by  injections  of 
strychnine  (1.5  mg.,  4V  E,^-),  and  (2)  by  inhalations  of  COj.  Both  of  these 
measures  seem  fairly  successful,  but  more  observations  are  necessary  be- 
fore conclusions  can  be  reached.  Pembrey  was  able  to  cause  the  periodic 
breathing  to  return  to  normal  by  causing  the  patient  to  breathe  either 
pure  O2  or  O2  containing  an  excess  of  CO2,  demonstrating  that  in  this 
case  the  action  of  the  respiratory  centre  could  be  restored  by  either  im- 
provin!^  its  condition  and  increasing  its  irritability  through  increased 
aeration,  or  by  increasing  the  strength  of  the  respiratory  stimulus  by  in- 
creasing the  concentration  of  CO2  in  the  lung  alveoli. 

The  occurrence  of  Cheyne-Stokes  respiration  is  a  very  grave  symptom. 
It  is  often  a  harbinger  of  death,  as  claimed  by  some  authors,  but  the  writer 
has  seen  many  patients  recover  from  it  and  even  live  for  several  years.  It 
should  therefore  be  classed  with  several  other  symptoms  as  indicating  a 
grave  weakening  of  the  circulation  but  not  necessarily  an  incurable  one. 

COUGH. 

Patients  with  chronic  cardiac  trouble  are  very  apt  to  suffer  from  a 
mild  cough,  even  during  their  periods  of  remission,  and  especially  every 
winter.  Sometimes  this  may  even  be  mistaken  for  a  primary  bronchitis. 
Primarily  the  condition  is  due  to  engorgement  of  the  pulmonary  vascular 
system,  with  increased  secretion  of  the  bronchial  mucous  glands  as  a  result. 
It  represents  a  state  of  mild  loss  of  pulmonary  compensation. 

In  somewhat  worse  form,  and  particularly  in  bad  cases  of  chronic  mitral  disease, 
the  alveolar  capillary  walls  become  so  much  injured  that  there  is  diapedesis  of  red  blood- 
cells  into  the  alveoli.  These  die  and  are  taken  up  by  phagocytes  which  find  their  way  into 
the  sputum  in  the  form  of  "  Herzfehlerzellen  " — large  endothelial  cells  containing  vacuoles 
and  numerous  brown  granules  of  hsemosiderin.  The  expectoration  of  "Herzfehlerzellen" 
is  usually  associated  with  a  condition  of  brown  induration  of  the  lungs,  a  chronic  interstitial 
pneumonia  with  dilatation  of  the  pulmonary  capillaries,  tortuous  condition  of  the  vessels, 
and  deposition  of  haemosiderin  in  the  tissues. 

ACCUMULATIONS   OF   FLUID   IN   CARDIAC  DISEASE. 

(Edema. — When  a  case  of  heart  disease  reaches  the  stage  of  broken 
(systemic)  compensation  and  the  right  heart  fails  to  perform  its  function 
properly,  cedema  of  the  feet  and  legs  sets  in.  This  occurs  at  some  stage 
of  almost  every  case  of  heart  disease,  but  not  always  at  stages  of  equal 
severity,  sometimes  setting  in  quite  early,  sometimes  only  as  a  terminal 
event.  Consequently,  although  a  grave  symptom,  the  presence  of  oedema 
need  not  indicate  a  desperate  condition. 

The  distribution  of  oedema  of  cardiac  origin  differs  characteristically 
from  the  nephritic  type.  This  is  readily  comprehensible  when  it  is  recalled 
that,  as  Cohnheim  has  shown,  oedema  occurs  only  when  there  has  been  some 
injury  to  the  walls  of  the  vessels  and  capillaries.  In  nephritis  Heinecke 
and  Meyerstein  have  proved  the  existence  of  a  substance  in  the  blood  which 


154 


DISEASES   OF   THE    HEART    AND    AORTA. 


injures  the  capillaries,  and  Kast  has  demonstrated  that  the  blood  of  nephrit- 
ics  contains  a  substance  with  lymphagogue  action.  As  might  be  expected 
from  a  poison  circulating  in  the  blood,  the  injury  occurs  simultaneously 
throughout  the  body.  Hence  in  nephritis  the  oedema  begins  quite  irre- 
spectively of  the  action  of  gravity  and  is  especially  marked  in  the  face  and 
eyelids.  In  cardiac  oedema  there  is  no  such  lymphagogue  poison  at  work, 
and  the  injury  to  the  capillary  w'alls  is  the  result  of  local  stasis,  lack  of 
oxygen  in  the  cells  of  the  capillary  walls  under  the  influence  of  the  slowed 
circulation.  Accordingly  it  begins  where  circulation  is  slowest,  i.e.,  in  the 
dependent  portions, — the  feet  and  legs, — and  either  remains  localized  there, 
or,  if  the  condition  becomes  worse,  progresses  upward  to  the  genitalia,  to 

the  abdominal  cavity  (portal  stasis), 
giving  rise  to  intense  ascites,  to  the 
subcutaneous  tissue  of  the  body  wall, 
and  finally  to  the  production  of  fluid 
in  the  chest  (hydrothorax). 

Occasionally  when  the  oedema  has  been 
long  continued  the  limbs  reach  tremendous 
proportions.  Some  four  years  ago  the  writer 
had  under  his  care  at  the  Johns  Hopkins 
Hospital  a  patient  who  reached  the  ward  in 
a  condition  of  very  marked  dyspnoea,  with 
legs  swollen  to  a  diameter  of  IQh  inches  and 
absolutely  elephantoid  in  appearance  (Fig. 
123).  The  skin  over  the  entire  legs  was  covered 
with  papillomatous  outgrowths  so  suspicious 
that  the  diagnosis  of  elephantiasis  vera  was 
seriously  entertained  by  some  members  of  the 
hospital  staff.  The  patient  had  been  suffering 
from  a  severe  aortic  insufficiency  for  about 
a  year,  and  for  six  months  had  been  so  ortho- 
pnoeic  that  he  had  not  been  able  to  go  to  bed, 
but  had  rested  sitting  bolt  upright  in  a  chair 
and  usually  with  feet  down.  There  were 
tremendous  crypt-like  ulcers  about  10  cm.  (4 
inches)  in  diameter  in  both  legs,  each  covered 
with  a  deep  layer  of  necrotic  tissue.  The  patient  was  placed  in  bed  with  feet  raised  to  the 
horizontal,  and  the  wound  dressed  with  a  1-10000  potassium  permanganate  solution  and 
tr.  digitalis  m.  xv  administered  every  four  hours.  He  was  purged  freely  with  Epsom  salts. 
He  improved  so  rapidly  that  within  twelve  hours  the  circumference  of  the  legs  had  appre- 
ciably diminished  and  within  a  few  weeks  they  were  almost  normal.  The  patient  has 
remained  quite  well  ever  since  and  is  at  present  managing  a  farm  in  western  Maryland. 

Unfortunately,  oedema  does  not  always  disappear  so  satisfactorily. 
It  has  been  shown  that  the  oedema  fluid  is  richer  in  salts  than  is  the  blood, 
and  that  resorption  of  the  oedema  is  somewhat  favored  by  a  practically 
salt-free  diet,  such  as  one  consisting  of  milk,  sugar,  eggs,  meats,  bread, 
sweet  butter,  and  cereals  prepared  without  the  addition  of  salt.  The  diu- 
retics, especially  those  of  the  caffein  group,  also  favor  resorption;^  free 

'  Fleisher,  Hoyt,  and  Loeb  have  shown  that  the  presence  of  calcium  salts  in  infusion 
fluid  diminishes  the  formation  of  oedema,  but  this  observation  had  not  yet  received  an 
application  in  therapeutics,  and  these  observers  have  found  that  this  does  not  apply  to 
cardiac  oedema. 


Fio.  123. — Legs  of  a  patient  with  extreme 
cedema  (simulating  elephantiasis)  and  tremen- 
dous ulcers.  Diameter  of  the  left  leg  lOJ  inches 
(25.5  cm.).  (Drawn  from  photographs  lent  by 
Dr.  W.  Preston  Miller,  of  Hagerstown,  Md.) 


SYMPTOMS   OF   CARDIAC   DISEASE. 


155 


iiS 


purgation  aids  in  removing  fluid  from  the  body,  sometimes  as  much  as  3000 
c.c.  per  day,  and  digitalis  does  the  same  by  increasing  heart  action.  Besides 
this,  the  oedema  can  be  combated  by  raising  the  legs  to  the  horizontal  or  if 
possible  a  little  above  it,  thereby  increasing  the  drainage  from  them. 

Drainage  of  Legs. — Sometimes  also  a  light  spiral  elastic  bandage  of  rubber  dam 
may  be  applied  to  the  legs,  beginning  at  the  feet  and  ascending  to  the  groin,  thereby 
assisting  the  drainage  and  replacing  the  lost  elasticity  of  the  skin.  When  these  means  are 
insufficient,  several  incisions  may  be  made  aseptically  in  the  skin  of  the  legs  and  drainage 
aided  by  applying  Bier's  suction  cups,  or  a  large  trocar  with  sides  perforated  (Curschmann's 
modification  of  Southey's  tubes)  may  be  inserted  to  bring  about  free  mechanical  drainage. 

The  best  results  are  obtained  by  the  following  method,  described  by  Romberg : 
Boil  a  long  rubber  tube  fitted  with  a  pinch-cock  in  physiological  salt  solution.  After 
removing  the  point  from  the  trocar,  attach  the  rubber  tube  to  the  metal  tube  of  the  latter 
and  place  the  lower  end  of  the  rubber  tube  in  a  basin 
of  boiled  water  upon  the  floor  next  to  the  bed.  In 
this  way  a  siphon  is  established,  helping  the  drainage 
of  the  fluid.  The  tube  of  the  trocar  should  be  kept 
in  place  in  the  leg  by  tying  with  a  silk  ligature,  the 
ends  of  which  are  then  inserted  in  a  strip  of  adhe- 
sive placed  loosely  about  the  leg  above  the* trocar. 
Romberg  states  that  from  2  to  15  litres  of  fluid  may 
be  removed  in  24  hours  ! 

The  cedema  often  involves  the  scrotum 
and  penis  until  they  are  enlarged  to  two  or 
three  times  the  ordinary  size,  and  phimosis 
or  paraphimosis  may  cause  considerable 
difficulty   in   micturition. 

Ascites.  —  Ascites  is  common  and  may 
cause  distress  by  pushing  up  the  diaphragm 
as  well  as  by  impeding  the  abdominal  circu- 
lation. It  is  often  advisable  to  remove  it 
mechanically  by  introducing  a  trocar  in  the 
midline  midway  between  the  umbilicus  and 

the  symphysis,  under  aseptic  precautions  (after  first  emptying  the  patient's 
bladder),  and  allowing  the  fluid  to  drain  out.  In  so  doing  care  must  be 
taken  to  keep  a  many-tailed  (Scultetus)  bandage  tight  across  the  abdomen, 
readjusting  it  several  times  during  the  tapping  for  fear  too  much  blood 
may  enter  the  relaxed  abdominal  vessels  when  the  pressure  about  them  is 
diminished  and  shock  result  therefrom  (see  page  31). 

Hydrothorax. — In  cases  wdth  severely  impaired  compensation  hydro- 
thorax  (usually  right  sided)  is  common.  Starling  and  Leathes,  Stengel,  and 
Dutton  Steele  have  demonstrated  that  its  frequency  upon  the  right  side  is 
due  to  the  position  of  the  great  azygos  vein,  which  drains  the  intercostal 
spaces  and  the  pleurse.  One  of  the  factors  producing  stasis  in  this  vein  is 
the  fact  that  the  latter  enters  obliquely  into  the  superior  vena  cava  (Fig.  5) 
and  thus  its  mouth  is  readily  closed  off.  Another  is  probably  the  fact, 
which  the  writer  has  noted,  that  the  mouth  of  the  vein  is  not  as  distensi- 
ble as  the  walls  of  the  vein  above  it,  and  hence  imposes  some  obstruction 
to  the  blood  flow.  In  all  cases  of  heart  failure  in  animals  the  azygos  vein 
may  be  seen  to  be  dilated  above  its  entrance  into  the  vena  cava.  The 
heart  in  hydrothorax  is  usually  displaced  to  the  left.    The  respiration  shows 


Fig.  124. — Curschmann's  modifica- 
tion of  the  Southey  tubes  for  draining 
oedema  of  the  legs.     (After  Romberg.) 


156  DISEASES   OF  THE   HEART   AND    AORTA. 

much  embarrassment:  (1)  from  removal  of  a  considerable  part  of  the 
right  lung,  (2)  from  compression  of  the  left  lung  by  the  displacement  of  the 
heart,  (3)  from  embarrassment  of  the  heart  itself  from  the  displacement, 
(4)  from  compression  of  the  venae  cavse  especially  during  defecation  and 
exertion.  This  may  prevent  inflow  into  the  heart  and  cause  sudden 
death.     (Calvert.) 

The  fluid  should  always  be  removed  promptly  by  paracentesis  thoracis. 
This  process  is  unfortunately  not  without  danger,  sudden  death  occasionally 
resulting  in  spite  of  the  greatest  care. 

The  writer  has  seen  two  deaths  of  this  kind,  and  they  occur  with  about  the  same 
frequency  in  the  experience  of  most  chnicians.  A  very  valuable  contribution  to  this  field 
has  been  made  by  the  studies  of  Capps  and  Lewis,  showing  that  the  visceral  layer  of  the 
inflamed  pleura  is  especially  sensitive,  and  upon  handling  or  touching  it  two  reflex 
phenomena  result,  a  vagal  inhibition,  sometimes  so  intense  as  to  stop  the 
heart,  and  a  paralysis  of  the  vasomotor  centre  which  gives  rise  to  a  marked  fall  of  blood- 
pressure.  According  to  these  observations  it  is  therefore  advisable  to  diminish  vagal  tone 
with  a  preliminary  hypodermic  injection  of  0.5  to  1  mg.  atropine  (gr.  xio  to  ^V)  about 
15  minutes  before  beginning  the  tapping,  and  to  have  at  hand  a  hypodermic  syringe  loaded 
with  1-10000  adrenalin  chloride  solution  to  restore  promptly  the  vasomotor  tone  in  case 
of  collapse. 

RENAL   COMPLICATIONS    OF   CARDIAC   DISEASES. 
RENAL  CHANGES. 

Albuminuria  and  diminished  secretion  of  urine  are  invariable  results 
of  broken  compensation.  They  may  also  occur  after  severe  exertion, 
probably  as  the  result  of  excessive  pressure  in  the  veins.  The  stasis  in  the 
vena  cava  and  renal  vein  has  been  shown  to  give  rise  to  albuminuria,  and 
the  slowing  of  the  circulation  through  the  kidney  is  sufficient  to  account 
for  the  diminution  of  the  urine  secreted.  Such  urine,  though  diminished 
in  amount,  is  highly  colored,  normal  or  increased  in  specific  gravity  (1016 
to  1026),  and  contains  a  normal  concentration  of  NaCl  and  urea.  The  total 
excretion  of  the  latter  in  24  hours  is,  of  course,  decreased.  As  in  the  experi- 
mental stasis  numerous  finely  granular  and  hyaline  casts  may  be  excreted. 

The  kidneys  of  such  cases  (Osier's  arteriosclerotic  kidneys)  are  usually  of  the  large 
red  or  "beefy"  type,  with  both  cortex  and  medulla  increased  in  size,  the  capsule  adherent, 
and  diffuse  interstitial  changes  as  well  as  some  parenchymatous  degeneration.  The  red 
color  is  probably  due  to  the  venous  congestion. 

It  is  of  great  importance  to  differentiate  between  a  primary  cardiac 
disease  with  secondary  renal  involvement  and  primary  chronic  nephritis 
with  secondary  arteriosclerosis,  cardiac  hypertrophy,  and  cardiac  insuffi- 
ciency. At  an  early  stage  of  the  disease  a  careful  study  of  the  chloride 
metabolism  and  its  relation  to  urine  concentration  may  be  of  great  help. 

In  cardiac  cases  the  power  of  excreting  NaCl  is,  as  a  rule,  not 
as  much  impaired  as  in  renal  cases.  If  5  Gm.  NaCl  be  added  to  the  diet  on 
one  occasion  there  should  be  an  abrupt  rise  in  the  NaCl  content  of  the  urine.  If  the  kidney 
cells  are  damaged  it  will  be  gradually  excreted  during  2-4  days.  However,  it  must  be 
remembered  that  in  many  cases  of  primarily  cardiac  origin  the  kidney  cells  may  be  im- 
paired. The  urinary  findings,  as  shown  in  the  cases  cited  on  page 
240  and  page  335,  may  be  practically  identical;  and  hence  all  the  fea- 
tures in  etiology,  history,  and  metabolism  must  be  thoroughly  considered  before  a  decision 
is  reached. 


SYMPTOMS   OF   CARDIAC   DISEASE. 


157 


SENSORY   SYMPTOMS   ABOUT  THE   HEART. 

Palpitation. — Under  normal  conditions  one  is  not  conscious  of  sensory- 
impressions  from  the  region  of  the  heart.  Einthoven,  Flohil,  and  Bat- 
taerd  have  shown,  however,  that  an  afferent  impulse  is  transmitted  up  the 
vagi  by  each  heart-beat,  and  there  are  probably  similar  impulses  transmit- 
ted through  the  intercostal  nerves  from  the  parietal  pleura,  mediastinum, 
and  chest  wall,  against  which  the  heart  is  beating.  Under  normal  condi- 
tions these  sensations  do  not  reach  consciounsess,  but  they  occasionally 
do  so  when  the  general  nervous  sensibility  is  increased,  as  by  coffee,  tobacco, 
or  hyperthyroidism,  in  neurasthenic  and  hysterical  states,  or  when  the 
beat  of  the  heart  is  more  forcible  than  usual.  The  distinct  sensation  caused 
by  each  beat  of  the  heart  is  known  as  palpitation.  It  is  frequently  associated 
with  cardiac  weakness  and  irregularities,  and  has  been  thought  by  some 
writers  to   be   clearly   associated  with  b 

extrasystoles.     But  while  it  is  true  that 


VAG. 


RESP. 


€AROT. 


Fig.  125. — Electrical  record  of  afferent  impulses  travelling  up  the  vagi.  (After  Einthoven,  Flohil, 
and  Battaerd.)  VAG.,  record  of  centripetal  electrical  wave  in  the  vagus  ;  RESP.,  respiration;  CAROT., 
carotid  tracing.  A.  In  quiet  breathing.  B.  In  apncea.  The  large  electrical  waves  are  due  to  respiration  ; 
the  small  ones  to  the  cardiac  contraction. 


extrasystoles  frequently  give  rise  to  palpitation  and  also  that  the  patient 
can  often  distinguish  between  strong  beats  and  weak  beats,  nevertheless 
there  are  many  cases  of  extrasystoles  without  palpitation  and  of  pal- 
pitation without  extrasystoles.  Hirschfelder  has  shown  that  palpitation 
may  occur  without  any  motor  disturbance  in  the  heart's  action  and  with- 
out any  change  in  the  reflex  response  of  the  heart  to  various  stimuli. 
Hewlett  has  found  the  c  wave  unusually  large  and  sudden  in  a  case  of 
palpitation,  and  believes  that  the  "earlier  movements  of  the  ventricle 
were  exerted  with  unusual  speed."  However,  this  finding  is  not  uniform 
in  cases  of  palpitation,  and,  moreover,  would  not  explain  the  occurrence  of 
palpitation  from  weak  extrasystoles  in  which  these  movements  are  executed 
slowly.  Such  changes  in  the  venous  pulse  are  often  found  in  vigorously 
beating  hearts  without  any  palpitation  whatever.  Palpitation  is  therefore  to 
be  regarded  as  a  purely  sensory  phenomenon,  which,  though  it  is  frequently 
associated  with  cardiac  disturbances,  may  occur  quite  independently. 

The  category  of  sensations  in  which  palpitation  should  be  placed  and  the  path  which 
the  sensation  traverses  are  not  perfectly  clear.  It  is  evidently  a  pressure  or  touch  sensation, 
perfectly  distinct  and  limited  to  the  period  of  systole.  It  is  always  sharply  locahzed, 
usually  referred  to  either  the  apex  or  the  bifurcation  of  the  trachea — the  two  sites  at  which 


158  DISEASES   OF  THE   HEART   AND    AORTA. 

the  heart  exerts  direct  pressure  or  traction  upon  the  surrounding  structures.  In  this  dis- 
tinctness it  differs  entirely  from  other  visceral  sensations,  which  are  less  definite  in  time 
and  in  site,  and  also,  as  a  rule,  more  nearly  allied  to  pain  sensation.  It  thus  differs  greatly 
from  the  pain  sensations  arising  in  and  about  the  heart,  and  hence  suggests  that  it  should 
be  placed  in  a  different  category.  Whether  the  path  of  the  sensation  is  up  the  vagi  or 
through  the  thoracic  nerves  cannot  at  present  be  stated.* 

Another  point  in  favor  of  the  view  that  palpitation  is  an  extracardiac  sensation  is  the 
fact  that  quite  similar  sensations  may  be  felt  in  the  abdominal  aorta  and  radial  arteries 
when  there  is  visible  pulsation  (to-and-fro  motion)  of  the  latter  with  pressure  and  traction 
upon  the  skin  and  surrounding  structures. 

The  continuance  of  the  sensation  is  very  wearing  upon  the  patient, 
especially  when  the  heart  is  irregular.  Often  he  is  able  to  distinguish  be- 
tween large  and  small  beats,  and  is  constantly  reminded  of  the  pathological 
condition  and  usually  much  worried  about  it.  The  sensation  is  not  entirely 
dependent  upon  psychic  phenomena;  for  in  one  case  under  the  writer's  obser- 
vation (I.e.)  it  disappeared  for  five  minutes,  while  the  blood-pressure  and  pulse- 
rate  rose  after  exercise  when  the  patient  was  under  examination,  although 
he  had  his  mind  fixed  upon  the  disturbance  throughout  the  entire  procedure. 

Palpitation  is  frequently  the  result  of  tea  or  coffee  drinking,  smoking, 
digestive  disturbances;  it  often  occurs  with  various  forms  of  cardiac  diseases, 
but  seems  to  have  no  relation  to  the  latter.  Relief  is  very  difficult  to  obtain. 
Except  for  removing  the  causal  factor,  application  of  an  ice-bag  or  a  cold- 
water  coil  over  the  heart  is  about  the  best  remedy.  The  bromides  of  potas- 
sium, ammonium,  and  strontium  are  of  some  value,  as  are  also  vibratory 
massage  and  the  application  of  sinusoidal  currents. 

Precordial  Pain.  —  Precordial  pain  is  a  less  definite  sensation  than 
palpitation.  It  is  continuous  throughout  the  cardiac  cycle,  is  less  definitely 
localized,  and  more  commonly  associated  with  referred  sensory  disturb- 
ances resembling  other  types  of  visceral  sensation.  It  seems  to  bear  a 
somewhat  closer  relation  to  dilatation  of  the  heart,  and,  as  a  rule,  accom- 
panies more  severe  organic  diseases,  being  especially  common  in  aortic  and 
mitral  lesions.    There  is  sometimes,  but  not  always,  precordial  tenderness. 

The  most  severe  form  of  precordial  pain,  angina  pectoris  (see  page 
285),  in  which  there  is,  besides  intense  pain,  a  feeling  as  though  the  heart 
were  held  in  a  vise,  seems  to  be  associated  with  sclerosis  of  the  coronary 
arteries,  but  a  definite  relation  between  this  and  other  forms  of  precordial 
pain  has  not  yet  been  established. 

Frequently  in  heart  diseases,  and  especially  in  cases  of  aneurism  and  angina,  there  is 
marked  pain  radiating  down  either  or  both  arms.  In  fact  these  may  be  the 
first  symptoms  given  by  an  aneurism.  It  is  easily  seen  from  the  distribution  of  the  cardiac 
nerves  (page  14,  Fig.  16)  that  a  lesion  in  the  vicinity  of  the  sympathetic  fibres  might  give 
sensations  which,  reaching  one  of  the  cervical  spinal  ganglia,  would  be  referred  to  its 
peripheral  distribution  in  the  cutaneous  region  innervated  by  that  segment,  usually  down 
the  arm.  Hence  the  frequency  of  these  pains.  Not  only  cardiac  condition,  but  high  blood- 
pressure  in  the  aorta  may  cause  this  distress.  It  is  difficult  to  relieve  this  symptom.  If 
lowering  of  the  blood-pressure  with  nitroglycerin  fails  to  bring  it  about,  codeine,  15  to 
20  mg.  {\  to  i  gr.)  should  be  tried,  and,  if  that  does  not  suffice,  morphine  may  have  to  be 
resorted  to,  but  should  always  be  avoided  as  long  as  possible. 

'  In  this  connection  it  would  be  interesting  to  note  whether  palpitation  occurs  in  cases 
of  transverse  lesion  of  the  cord  in  the  lower  cervical  or  upper  thoracic  region,  or  whether 
it  can  be  brought  on  in  such  persons  by  large  doses  of  coffee. 


SYMPTOMS   OF   CARDIAC   DISEASE.  159 


DIGESTIVE   DISTURBANCES. 

One  of  the  first  effects  of  weakening  of  the  heart  is  engorgement  of 
the  veins  of  the  portal  system,  and  this  in  turn  brings  about  a  catarrhal 
condition  in  the  mucosa,  and  especially  the  gastric  mucosa,  with  consequent 
symptoms  of  indigestion.  Fermentation  frequently  takes  place,  and  the 
inflation  of  the  stomach  with  gas,  displacing  the  diaphragm  upwards  and 
shifting  the  heart  more  towards  the  horizontal,  tends  to  increase  its  embar- 
rassment. Overloading  the  stomach,  the  transdiaphragmatic  neighbor 
of  the  heart,  should  therefore  always  be  avoided;  and  the  patient  will  be 
saved  much  suffering  if  he  is  kept  on  a  light,  easily  digestible  diet,  consist- 
ing largely  of  eggs,  milk,  and  carbohydrates,  just  enough  in  quantity  to 
keep  him  from  losing  weight.  Friedrich  Miiller  has  shown  a  diminished 
power  of  absorption  of  fats  in  heart  disease.  Perhaps  this  may  be  due  to 
the  fact  that  the  high  venous  pressure  prevents  the  thoracic  duct  from 
emptying  itself  properly,  or  perhaps  because,  as  H.  M.  Evans  has  shown, 
a  high  portal  pressure  causes  the  lymphatics  of  the  intestines  to  collapse. 

On  the  other  hand,  meats  and  other  foods  containing  purin  bodies  in 
large  quantities  (sweetbreads,  lungs,  liver,  etc.,  also  coffee  and  tea,  and 
alcohol  in  all  forms)  do  distinct  harm  by  raising  the  blood-pressure  and  by 
increasing  the  viscosity  of  the  blood  (page  39). 

The  engorgement  of  the  gastric  and  oesophageal  veins  sometimes  leads 
to  exudation  of  blood  into  the  stomach  and  to  vomiting  of  blood. 

Abdominal  Pain  from  Distended  Liver. — One  of  the  commonest  symp- 
toms of  failing  compensation  is  very  intense  abdominal  pain  felt  over  the 
region  of  the  liver.  This  organ  may  become  much  distended,  and,  as  shown 
by  Salaman,  may  be  expanded  until  its  blood  content  is  several  degrees 
above  the  normal.  Under  this  expansion  there  is  marked  tension  upon 
the  capsule  of  the  liver  (Glisson's  capsule)  which,  in  turn,  gives  rise  to 
pain.  This  symptom  is  really  so  clearly  bound  up  with  the  failure  of  com- 
pensation itself  that  it  subsides  with  resumption  of  the  latter,  or  after  some 
time  the  capsule  of  the  liver  will  have  become  sufficiently  stretched  and  it 
will  then  cease  to  be  painful. 

Abdominal  pain  also  results  from  arteriosclerosis  of  the  gastric  and 
mesenteric  arteries,  from  vascular  crises  as  well  as  from  abnormally  great 
pulsation  of  the  abdominal  aorta. 

Catarrhal  Jaundice. — Like  the  gastric  mucosa,  the  bile  passages  undergo 
catarrhal  inflammation  from  the  venous  engorgement,  and  a  definite 
catarrhal  jaundice  may  accompany  the  failure  of  compensation.  Usually, 
the  jaundice  is  mild  and  barely  perceptible,  the  color  being  sallow  and  icte- 
roid  rather  than  icteric.  The  presence  of  this  slight  icteric  hue  in  a  patient 
with  heart  disease  should  always  lead  to  the  suspicion  of  broken  compen- 
sation or  tricuspid  insufficiency,  and  is  always  a  sign  of  danger. 

PSYCHIC    DISTURBANCES. 

An  anxious  expression  is  so  commonly  manifested  by  patients  suffer- 
ing from  heart  disease  that  a  certain  type  is  spoken  of  as  "the  cardiac 
facies."    This  facies  is  difficult  to  describe,  but  may  be  said  to  be  character- 


160  DISEASES   OF   THE    HEART   AND    AORTA. 

ized  by  bright  watery,  somewhat  staring  eyes,  wide  palpebral  slits  (without 
definite  exophthalmus  or  other  signs  of  Basedow's  disease),  rather  tensely 
held  mouth,  and  the  rest  of  the  face  a  little  sunken,  though  not  to  the  degree 
present  in  the  "abdominal  facies."  Many  cardiac  cases,  perhaps  from  the 
difficulty  which  they  are  constantly  experiencing  in  getting  their  breath,  feel 
irritable  and  peevish  to  a  considerable  degree,  and  not  infrequently  the  onset 
or  increase  of  peevishness  is  an  early  sign  that  the  cardiac  condition  has 
become  worse. 

DELUSIONS. 

Occasionally,  especially  in  patients  with  irregular  heart  action,  definite 
psychoses  set  in.  These  are  especially  common  during  the  night  and  early 
morning,  disappearing  again  during  the  waking  hours. 

The  patient  usually  awakens  from  his  sleep  unable  to  recognize  the  place  where  he  is, 
which  he  usually  locates  somewhere  else,  and  then  regards  the  doctors,  nurses,  and  attend- 
ants as  inhabitants  of  the  more  familiar  scenes,  often  mistakenly  recognizing  them  as 
people  of  his  acquaintance  in  those  places.  He  usually  regards  his  confinement  in  bed  as 
a  sign  of  some  attempt  upon  his  life,  and  the  administration  of  medicine  as  a  certain  at- 
tempt to  poison  him.  Of  this  fact  he  is  always  certain,  although  he  may  admit  that  there 
is  some  doubt  in  his  own  mind  as  to  the  correctness  of  some  of  his  other  ideas.  For 
example,  one  deUrious  patient  under  the  writer's  care  as  house  physician  mistook  him  for 

an  old  friend  from  home  and  said,  "  He  liked ,  and  had  great  confidence  in  him,  but 

he  could  not  see  why did  want  to  poison  him."     But  he  would  recognize  no  other 

possible  motive. 

Occasionally  when  daylight  comes  or  some  one  familiar  object  appears,  the  patient 
suddenly  recognizes  his  surroundings,  wakes  up  as  from  a  dream,  and  may  even  e^cplain 
exactly  the  nature  of  and  reasons  for  his  delusions.  Under  the  influences  of  these 
delusions,  patients  are  often  very  hard  to  manage,  but  their  attitude  is  more  commonly  a 
defensive  than  an  offensive  one,  resisting  confinement  and  treatment,  and  attempting  to 
leave  the  ward  or  room  peaceably,  rather  than  showing  maniacal  pugnaciousness  primarily. 
They  can  usually  be  i^ersuaded  by  gentle  means  to  remain  where  they  are  for  a  time, 
especially  as  their  minds  are  almost  always  confused  ;  they  realize  that  they  are  not 
perfectly  well,  and  the  nurse  or  physician  can  lead  the  argument  along  its  logical 
conclusions  to  a  reason  why  they  should  return  to  bed  and  to  rest  for  the  time  being. 
After  some  minutes'  argument  of  this  kind  the  patient  can  usually  be  given  a  hypo- 
dermic of  morphine  and  gotten  back  to  bed  with  much  less  injury  to  himself  than  if 
forcible  means  were  attempted.  He  can  then  usually  be  kept  in  bed  by  an  attendant 
constantly  present. 

The  reason  for  these  delusions  is  not  very  certain,  but  in  some  cases 
they  may  be  regarded  as  "waking  dreams"  not  very  different  from  those 
of  somnambulists,  and  perhaps  like  the  night  terrors  of  children  with  ade- 
noids. They  may  be  asphyxial  in  origin,  associated  more  or  less  with 
cerebral  arteriosclerosis  and  cerebral  anaemia,  of  which  perhaps  the  frequent 
high  blood-pressure  may  be  another  expression.  This  delusional  insanity  is  a 
bad  omen,  and  its  onset  often  precedes  the  fatal  outcome  by  only  a  few  days 
or  weeks.  Duroziez  and  H.  O.  Hall  have  called  attention 
to  the  fact  that  in  some  cases  these  delusions  may  be 
due  solely  to  the  digitalis  and  may  disappear  entirely  when  the 
drug  is  discontinued. 

H.\LLUCINATIONS. 

Definite  hallucinations  of  sight  and  hearing  are  also  not  uncommon. 

Henry  Head  has  observed  that  these  are  especially  common  in  aortic  disease  about 
the  time  of  twilight,  and  are  usually  quite  simple  in  character,  the  auditory  hallucinations 


SYMPTOMS   OF   CARDIAC   DISEASE.  161 

consisting  in  simple  rhythmic  sounds  (associated  with  the  heart-beats?),  such  as  of  knock- 
ing or  of  bells  tolling,  the  visual  hallucinations  usually  taking  the  form  of  the  face 
of  a  man  or  woman  seen  stationary  at  the  foot  of  the  bed  or  slowly  stalking  across 
the  room.  The  face  is  ashy  white,  the  eyes  black  and  staring,  and  the  contour  invariably 
indefinite  and  surrounded  by  a  mass  of  wavy  black  hair.  If  the  body  is  seen  at  all,  it  is 
poorly  outlined  as  though  draped  in  a  black  gown.  Head  found  this  hallucination  quite 
constant  and  seen  by  many  patients,  though  they,  as  a  rule,  recognized  the  hallucinatory 
character  and  spoke  of  it  only  after  the  physician  had  gained  their  confidence.  Thewi'iter 
has  also  elicited  the  same  answers  from  a  number  of  patients,  after  prefacing  the  question 
by  a  statement  that  visual  hallucinations  were  not  uncommon  in  their  disease  and  were 
to  be  regarded  merely  as  troublesome  but  not  significant  features  of  the  disease  itself. 
All  who  gave  positive  answers  accurately  described  the  hallucinatory  \dsion  as  above. 

Head  states  that  highly  colored  and  rapidly  moving  visions  do  not 
occur  frequently  in  heart  cases,  but  the  writer  has  seen  one  very  marked 
exception  to  this  rule. 

This  was  in  the  case  quoted  on  page  508 — a  young  railroad  engineer,  23  years  old, 
of  temperate  habits  and  excellent  family  history,  who  had  a  very  adherent  pericardium. 
For  several  years,  especially  when  his  cardiac  condition  became  worse,  he  suffered  from 
seeing  a  few  feet  before  him  swarms  of  large  animals,  lions,  tigers,  etc.,  all  highly  colored, 
leaping  rapidly  about.  He  recognized  these  as  hallucinations  at  the  time,  but  stated  that 
the  sight  irritated  him  so  that  he  lost  his  self-control,  and  he  begged  to  be  placed  in  soli- 
tary confinement  for  a  few  days  until  the  hallucinations  passed  off.  He  was  then  once 
more  a  perfectly  rational  being.. 

Like  the  delusions,  these  cardiac  hallucinations  are  probably  due 
either  to  anaemia  or  venous  stasis  in  brain,  but  especially  in  the  special 
centres,  or  in  the  retina,  middle  ear,  visual  or  auditory  centres,  .giving  rise 
to  rudimentary  sensations  which  the  mind  translates  or  distorts  into  the 
above-mentioned  pictures. 

Syncopal  attacks  also  occur  in  some  forms  of  heart  disease  as  a  result 
of  cerebral  anaemia  and  will  be  discussed  in  detail  in  Part  III,  Chapter  XI, 
under  the  head  of  Adams-Stokes  disease.  The  feeling  of  faintness  and 
weariness  unaccompanied  by  syncope  will  be  discussed  under  "  cardiac 
neuroses,"  etc.  (Part  IV,  Chapter  III), 

BIBLIOGRAPHY. 
Symptoms  of  Cardiac  Disease. 

Grossmann,  Bettelheim,  and  Kauders.    Quoted  on  page  146. 

Eyster,  J.  A.  E.:  Clinical  and  Experimental  Observations  upon  Cheyne-Stokes  Respira- 
tion, J.  Exper.  Med.,  N.  York  and  Lancaster,  1906,  viii,  265. 

Welch,  1.  c,  page  145. 

Emerson,  H.:  Artificial  Respiration  in  the  Treatment  of  CT^dema  of  the  Lungs.  A  Sug- 
gestion based  on  Animal  Experimentation,  Arch.  Inter.  Med.,  Chicago,  1909,  iii,  368. 

Barringer,  T.  B.:  Pulmonary  CEdema  Treated  by  Artificial  Respiration,  Report  of  a  Case; 
ibid.,  1909,  iii,  372. 

Miller,  J.  L.:  Trans.  Assoc.  Am.  Phys.,  Pliila.,  1909.  Also,  Miller,  J.  L.,  and  Matthews, 
S.  A.:  A  Study  of  the  Mechanical  Factors  in  Experimental  Acute  Pulmonary  CEdema, 
Arch.  Int.  Med.,  Chicago,  1909,  iv,  356. 

Miiller,  Fr.:  Die  Erkrankungen  der  Bronchien,  Die  deutsche  Klinik.,  Berl.  and  Vienna, 
iv,  279;    quoted  from  Romberg. 

Mosso,  A.:  Fisiologia  dell  roma  sulla  Alpi,  Arch.  Ital.  de  Biol.,  1905,  xliii;  and  other 
articles  quoted  on  page  35. 

Pembrey,  M.  S.,  Beddard,  A.  P.,  and  French,  H.:  Observations  on  Two  Cases  of  Cheyne- 
Stokes  Respiration,  Proc.  Physiol.  Soc,  Lond.,  1906,  p.  vi. 
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162  DISEASES   OF   THE   HEART   AND   AORTA. 

Kast,  A.:  Ueber  lymphagoge  Stoffe  im  Blutserum  Nierenkranken,  Deutsch.  Arch.  f.  klin. 

Med.,  Leipz.,  1902,  Ixxiii,  562. 
Heineke  and  Myerstein:  Experimentelle  Untersuchungen  ueber  den  Hydrops  bei  Nieren- 

krankheiten,  Deutsch.  Arch.  f.  klin.  Med.,  Leipz.,  1908,  xcii,  101. 
Fran^ois-Franck,   Ch.   A.:  Contribution   a  I'etude   experimentale   des  nevroses    reflexes 

d'origine  nasale.  Arch,  de  physiol.  des  hommes  et  des  anim,  Par.,  1889,  oe  s6r.,  i,  538. 
Starling,  E.  H.:  Physiologic  Factors  Involved  in  the  Causation  of  Dropsy,  Lancet,  Lond., 

1896,  cl,  1407. 
Meltzar,  S.  J.:  (Edema,  Am.  Med.,  Phila.,  1904,  iii,  19,  59,  151,  161. 
Pearce,  R.  M.:  The  Production  of  (Edema,  Arch.  Int.  Med.,  Chicago,  1909,  iii,  423. 
Pearce,  R.  M.:  An  Experimental  Study  of  the  Influence  of  Kidney  Extracts  and  of  the 

Serum  of  Animals  with  Renal  Lesions  upon  Blood-pressure,  J.  Exper.  M.,  1909,  xi,  430. 
Fleisher,  M.  S.,  Hoyt,  D.  M.,  and  Loeb,  L.:  Studies  in  QMema.    I.  Comparative  Investi- 
gation into  the  Action  of  Calcium  Chloride  and  Sodium  Chloride  on  the  Production 

of  Urine,  Intestinal  Fluid,  and  Ascites,  J.  Exper.  Med.,  N.  York  and  Lancaster,  1909, 

xi,  291. 
Fleisher,  M.  S.,  and  Loeb,  L.:  The  Influence  of  Myocarditic  Lesions  on  the  Production  of 

Ascites,  Intestinal    Fluid,  and  Urine  in  Animals  infused  with   Solutions  of  Sodium 

Chloride  and  of  Sodium  Chloride  and  Calcium  Chloride,  J.  Exper.  Med.,  N.  York  and 

Lancaster,  1909,  xi,  480. 
Romberg,  E.:  Lehrbuch  der  Krankheiten  des  Herzens  und  der  Blutgefasse,  Stuttgart, 

1906. 
Capps,  J.  A.:  Some  Observations  on  the  Effect  on  the  Blood-pressure  of  Withdrawal  of 

Fluid  from  the  Thorax  and  Abdomen,  J.  Am.  M.  Assoc,  Chicago,  1907,  xlviii,  22. 
Starling,  E.  H.,  and  Leathes,  J.  B.:  The  Arris  and  Gale  Lectures  on  Some  Points  in  the 

Pathology  of  Heart  Disease,  Lancet,  Lond.,  1897,  i,  569. 
Stengel,  A.:  Right-sided  Cardiac  Hydrothorax,  Univ.  Penn.  M.  Bull.,  Phila.,  1901,  xiv, 

103. 
Steele,  J.  D.:  Pleural  Effusion  in  Heart  Disease,  J.  Am.  M.  Assoc,  Chicago,  1904,  xliii, 

927. 
Calvert,  W.  J. :  Sudden  Death  in  Pleurisy  with  Effusion  due  to  Change  of  Position,  Johns 

Hopkins  Hosp.  Bull.,  Bait.,  1908,  xix,  44. 
Capps,  J.  A.,  and  Lewis,  D.  D.:  Observations  upon  Certain  Blood-pressure-lowering  Re- 
flexes that  Arise  from  Irritation  of  the  Inflamed  Pleura,  Am.  J.  M.  Sc,  Phila.  and 

N.  Y.,  1907,  cxxxiv,  868. 
Einthoven,  W.,  Flohil,  A.,  and  Battaerd,  P.  J.  T.  A.:  On  Vagus  Currents  Examined  with 

the  String  Galvanometer,  Quart.  J.  Exper.  Physiol.,  Lond.,  1908,  i,  243.    Ueber  Vagus- 

strome.  Arch.  f.  d.  ges.  Physiol.,  Bonn,  1909,  cxxiv,  246. 
Hirschfelder,  A.  D.:  Observations  on  a  Case  of  Palpitation  of  the  Heart,  Johns  Hopkins 

Hosp.  Bull.,  Bait.,  1906,  xvii,  299. 
Hewlett,  A.  W.:  The  Venous  Pulse,  Science,  Lancaster,  1909,  xxix,  515. 
Miiller,  F.     Quoted  from  Romberg. 
Evans,  H.  M.:  Personal  communication. 

Salaman,R.  N.:  The  Pathology  of  the  Liver  in  Cardiac  Disease,  Lancet,  Lond.,  1907,  i,  4. 
Duroziez,  P.:  Du  d^lire  et  du  coma  digitaliques,  Gaz.  hebdom..  Par.,  1874,  xi,  780. 
Hall,  H.  O.:  The  Hallucinations  of  Digitalis:  Does  Digitalis  Cause  Hallucinations,  Delir- 
ium, or  Insanity  under  Certain  Conditions?     Am.  Med.,  Phila.,  1901,  i,  598.     The 

Delirium  and  Hallucinations  of  Digitalis,  ibid.,  1905,  ix,  489. 
Head,  H.:  Certain  Mental  Changes  that  Accompany  Visceral  Disease;   Brain,  Lond.,  1901, 

xxiv,  345. 


IV. 

GENERAL  PRINCIPLES  OF  TREATMENT  OF  FAILURE 
OF  THE  HEART. 

The  best  index  of  the  treatment  of  the  patient  is  his  own  condition, 
sensations,  and  general  appearance.  Physical  examinations,  determina- 
tion of  blood-pressure  and  pulse-rate,  as  well  as  of  increase  in  the  product 
of  pulse-pressure  by  pulse-rate  (velocity  coefficient),  venous  tracings,  and 
gas  analysis  aid  in  the  interpretations  of  the  condition,  and  particularly 
in  discovering  where  the  fault  in  the  mechanism  of  the  circulation  lies; 
but  the  changes  of  conditions  themselves  are  often  very  subtle  and  mani- 
fest themselves  in  the  general  condition  of  the  patient  before  they  can  be 
detected  on  examination. 

QUIET. 

The  most  important  element  in  the  treatment  of  cardiac  failure  is 
rest  as  complete  as  possible.  In  all  cases  of  heart  failure  or  disease  in  the 
heart  the  patient  should  be  confined  to  bed,  if  necessary  propped  up  with 
pillows,  and  should  be  kept  there  until  the  acute  symptoms  have  subsided 
and  have  remained  quiescent  for  several  days. 

As  Morton  Prince  has  shown,  mental  excitement  and  worry  are  impor- 
tant factors  in  bringing  about  acute  dilatation  of  the  heart;  but  they  are  usually 
contributing  factors  rather  than  sole  causes. 

The  effect  of  mental  activity  upon  the  circulation  is  to  bring  about  vasoconstriction, 
of  both  extremities  and  viscera,  a  slight  rise  of  blood-pressure,  and  increase  in  the  pulse- 
rate;  all  of  which  taken  together  considerably  increase  the  total  work  of  the  heart  {i.e., 
roughly  speaking,  the  product  of  maximal  pressure  by  pulse-rate). 

A  good  night's  sleep  is  often  the  best  remedy  for  the  patient  with  a 
weak  heart,  and  almost  any  method  by  which  it  may  be  procured  may  prove 
a  good  therapeutic  procedure.  Small  doses  of  bromides,  if  necessary  aided 
by  a  little  trional,  veronal,  or  other  hypnotic,  often  suffice  for  this  purpose 
and  allow  the  heart  a  few  hours  respite  in  which  the  other  therapeutic 
measures  may  have  opportunity  to  act. 

However,  it  must  be  borne  in  mind  that  in  persons  who  are  much 
worried,  mental  rest  and  absence  of  distractions  or  occu- 
pation are  not  necessarily  synonymous.  Indeed,  the  removal 
of  other  subjects  for  thought  may  serve  only  to  centre  the  patient's  mind 
upon  himself  and  his  ailments  and  may  increase  rather  than  diminish  the 
nervous  strain.  This  should  be  carefully  guarded  against.  The  daily  routine 
should  therefore  be  accommodated  to  both  the  general  condition  and  the 
temperament  of  the  patient.  If  possible  absolute  rest  and  isolation  should 
be  secured  for  the  worst  cases  of  heart  failure,  but  even  for  these  patients 
a  few  minutes'  conversation  with  a  cheerful  friend,  whose  demeanor  is  quiet 
and  soothing,  may  be  of  actual  benefit.    Reading  should  not  be  allowed  to 

163 


164  DISEASES   OF   THE   HEART   AND    AORTA. 

patients  in  the  worst  stages,  but  a  little  reading  of  the  lightest  and  least 
exciting  sort  may  otherwise-  be  allowed. 

Rest,  Distraction,  and  Spa  Treatment. — As  Mackenzie  states,  it  is  chiefly 
due  to  the  element  of  mental  distraction  combined  with  the  judicious 
supervision  of  a  physician  and  the  favorable  climatic  conditions,  which 
make  the  Spa  treatments  of  cardiac  disease  so  successful;  although,  as 
he  states,  each  Spa  physician  has  evolved  some  method  of  treatment  which 
he  regards  as  of  special  benefit,  when  the  actual  benefit  has  been  due  to  the 
air  and  restfulness  itself.  Nevertheless,  it  must  be  confessed  that  the  treat- 
ments at  Nauheim  by  the  late  August  Schott  (page  194)  have  been  of  great 
benefit,  and  being  founded  upon  sound  physiological  doctrines  have  been 
applicable  elsewhere  as  well.  The  physician  must  always  realize  that, 
however  little  there  may  be  in  the  Spa  treatments  ptr  se,  the  combination 
of  the  mental  rest  and  change  of  air  with  the  baths  and  dietetic  treatment 
is  one  which  the  patient  whose  condition  warrants  a  trip,  should  not  forego. 

Rest  in  Bed. — The  bed  should  not  be  so  high  above  the  floor  as  to  make 
it  hard  to  get  in  and  out;  it  should  if  possible  have  a  metal  frame  and  a  good 
rather  firm  mattress.  It  should  be  provided  with  a  good  back  rest  ready 
for  use  in  case  the  patient  finds  it  more  comfortable,  and  plenty  of  pillows 
should  be  available. 

In  dealing  with  cases  of  mild  cardiac  failure  it  may  be  impossible  in 
private  practice  to  compel  the  patients  to  remain  in  bed  all  the  time,  and 
then  it  may  suffice  to  insist  upon  their  lying  down  for  several  hours  a  day 
without  absolutely  remaining  in  bed.  Under  these  circumstances  the 
physician  must  insist  that  the  patient  remain  quiet  all  day  upon  a  sofa 
or  in  a  wheel  chair  with  legs  raised.  A  short  period  of  such  absolute  rest 
is  better  than  a  much  longer  period  of  relative  invalidism,  for  it  enables 
the  dilated  heart  to  bail  itself  out,  to  regain  its  former  dimensions  and 
tonicity,  and  permits  the  heart-rate  to  return  to  normal.  It  is  important 
that  the  patient  should  remain  horizontal  rather  than  in  sitting  or  in  stand- 
ing posture,  since  the  latter  tends  to  slow  the  circulation  (cf.  Erlanger  and 
Hooker,  quoted  on  page  26) .  The  rest  should  continue  until  all  symptoms 
have  subsided,  until  cardiac  distress,  pain,  and  palpitation  have  disappeared, 
and  respiration  has  again  returned  to  normal.  If  possible  the  subsidence 
of  tachycardia  or  irregularity  of  the  pulse  should  be  awaited ;  but  these  may 
persist  for  some  time  even  in  spite  of  the  improvement  in  the  patient's 
general  condition,  and  may  have  to  be  disregarded.  After  the  symptoms 
have  subsided  (in  severe  cases  after  the  symptoms  have  remained  quies- 
cent for  a  few  days),  the  patient  may  be  allowed  to  get  out  of  bed  and  sit 
up  in  an  arm  chair  or  wheel  chair  for  a  little  while.  At  first  this  period 
should  be  very  short,  to  avoid  exhaustion,  but  it  may  be  gradually  increased 
and  he  may  soon  be  allowed  to  walk.  (For  exercises  to  be  taken  by  patient 
with  cardiac  disease  see  page  199.) 

COLD    APPLICATIONS    OVER   THE    HEART. 

The  application  of  cold  to  the  precordium  is  of  value  both  for  the 
cardiac  symptoms  (palpitation  and  pain)  on  the  one  hand,  and  for  diminu- 
tion of  the  heart-rate  on  the  other.    This  may  be  carried  out  by  the  applica- 


TREATMENT   OF   FAILURE   OF   THE   HEART.  165 

tion  of  a  simple  ice-bag  (especially  containing  a  mixture  of  ice  and  salt) 
which  may  be  kept  in  close  application  to  the  skin  by  tying  it  around  the 
chest  and  shoulders  with  a  strong  elastic  four-tailed  bandage.  The  ice-bag 
should  be  changed  every  hour  or  two  in  order  to  keep  up  an  intense  cooling.^ 

In  hospital  use  or  in  well-supplied  houses  the  use  of  the  cardiac  tube  is  most  satisfac- 
tory. This  consists  of  a  coil  of  thin-walled  rubber  or  aluminum  tube  applied  over  a  wet 
compress  to  the  precordium.  A  stream  of  cold  water  from  a  cooler  is  kept  (lowing  slowly 
through  the  tube.  The  cooling  of  the  skin  thus  obtained  is  excellent  and  without  any 
discomfort  to  the  patient.  Its  effects  have  been  tested  both  clinically  and  experimentally 
by  Wintemitz  and  da  Silva. 

These  observers  found  that  the  application  of  cold  to  the  precordium  brought  about 
in  dogs  a  cooling  of  both  the  anterior  and  posterior  surfaces  of  the  pericardium,  amount- 
ing to  l°-5°,  and  was  accompanied  by  a  slowing  of  the  pulse  and  rise  of  blood-pressure 
from  120  to  190  mm.  Hg.  In  man  the  pulse-rate  did  not  begin  to  fall  for  fifteen  minutes 
after  the  application,  and  reached  its  height  within  an  hour,  lasting  in  turn  about  an  hour 
after  removal  of  the  cold.  In  normal  individuals  they  found  the  pulse-rate  falling  from 
72  to  64,  68  to  52,  78  to  68;  in  other  cases,  chlorosis  84  to  72,  pericarditis  84  to  78,  mitral 
stenosis  60  to  40.  Simultaneously  the  blood-pressure  rises  and  the  pulse  increases  in  vol- 
ume. There  is  evidently  both  a  reflex  vasoconstriction  from  stimulation  of  the  vasomotor 
centre  and  a  reflex  stimulation  of  the  vagus.  Besides  this,  da  Silva  thinks  that  there  is  a 
direct  stimulation  of  the  heart  muscle.  It  will  be  noted  that  these  effects  are  exactly  those 
brought  about  by  digitalis,  and  hence  enthusiastic  hydrotherapists  are  in  the  habit  of 
speaking   of  the   ice-bag  as    "physiological   digitalis.'' 

Its  use  is  attended  with  less  danger,  but  in  cases  of  extreme 
fibrous  or  fatty  degeneration  of  the  heart,  cyanosis 
and  collapse  occasionally  occur.  Hence  it  should  be  ap- 
plied very  mildly  in  cases  where  these  conditions  are  suspected. 

There  can  be  no  doubt  that  the  ice  application  is  not  as  efficient  as  the  use  of  digitalis 
in  slowing  and  strengthening  the  heart,  but  when  the  two  are  vigorously  used  at  the  same 
time  they  may  greatly  reinforce  one  another,  and  the  vigorous  use  of  a  good  ice-bag  may 
enable  satisfactory  effects  to  be  obtained  with  smaller  doses  of  digitalis  than  would  other- 
wise suffice. 

VENESECTION. 

When  the  patient  is  in  very  bad  condition,  deeply  cyanotic,  and  rest- 
less or  nervous,  and  the  area  of  cardiac  dulness  is  increased  to  the  right, 
a  free  venesection  will  often  bring  the  greatest  relief.^ 

Technic  of  Venesection.  —  Venesection  is  best  performed  in  the  following  manner: 
The  skin  over  the  flexor  surface  of  the  elbow-joint  is  scrubbed  with  green  soap  and  washed 
with  warm  water,  then  with  alcohol,  and  lastly  with  1-2000  bichloride  solution.  An  elastic 
or  gauze  bandage  is  tied  about  the  upper  arm  tightly  enough  to  cause  the  veins  to  stand  out 
but  not  to  obliterate  the  pulse  at  the  wrist.  The  largest  vein  visible  (usually  the  median 
cephalic)  is  selected  and  a  small  slit  in  the  skin  just  alongside  of  (not  over)  the  vein  is  made 
with  a  curved  bistoury,  which  is  then  pushed  in  through  the  slit  in  the  skin  and  under  the 
vein.  It  is  then  twisted  so  that  the  edge  is  turned  upward  towards  the  skin  against  the 
vein  and  the  vein  cut  through  without  again  piercing  the  skin.  A  very  free  flow  of  blood 
is  obtained,  especially  by  keeping  the  arm  dependent  and  if  the  patient  is  made  to  clench 
and  open  his  hands  rapidly.  From  300  to  1200  c.c.  (12  ounces  to  2^  pints)  can  thus  be 
removed  in  less  than  twenty  minutes,  usually  with  great  relief  to  the  patient.     Breathing 

'  When  a  mixture  of  ice  and  salt  is  used  it  is  possible  to  actually  freeze  the  skin,  an 
accident  which  must  be  carefully  avoided. 

^  The  haemoglobin  should  always  be  tested  before  performing  a  venesection;  and  it 
should  not,  as  a  rule,  be  performed  if  the  haemoglobin  is  below  70  per  cent. 


166 


DISEASES    OF   THE   HEART    AND    AORTA. 


becomes  easier,  the  head  clearer,  and  the  general  condition  better,  but  the  crucial  point  is 
reached  when  the  color  changes  and  the  cyanosis  gives  way  to  a  healthy  rosy  color  in  the 
lips  and  elsewhere.  This  indicates  that  the  overstrained  heart  has  been  unburdened,  and 
the  bleeding  need  not  be  pushed  much  further.  Indeed  it  should  not  be,  for  to  cause  an 
anaemia  is  dangerous.     All  that  is  desired  is  to  relieve  the  distention  of  the  right  heart. 


Fig.  126. — Insertion  of  the  knife  in  venesection.     A.  Lateral  view.     B.  Cross  section  of  arm. 

Effect  of  Venesection  on  the  Circulation. — The  value  of  venesection  can  often  be  seen 
in  experiments  upon  animals.  It  is  not  at  all  uncommon  to  find  a  heart  faiUng  and  an 
auricle  already  paralyzed  from  overdistention,  in  which  a  free  venesection  gives  immediate 
relief,  and  the  auricle  as  w^ell  as  the  ventricle  resumes  forcible  contractions.  The  effect  of 
this  procedure  upon  the  blood-pressure  is  variable  and  depends  to  a  certain  extent  upon 
the  phenomena  present  before  the  venesection. 


Before  Venesection. 

After  Venesection. 

Blood-pressure. 

Condition. 

1.  Normal  or  elevated 

2.  High 

Heart  distended  but  circulation 
still  sufficient 

Circulation  slowed.  Vasocon- 
striction through  stimulation 
of  medulla  by  excess  of  COj 
in  the  blood 

Circulation  slowed;  heart  fail- 
ing. Unable  to  keep  up  cir- 
culation through  medulla  in 
spite  of  vasoconstriction 

Fall  of  blood-pressure  from  emp- 
tying of  vascular  system  and 
diminished  viscosity  of  blood.' 

Fall  of  blood-pressure;   occasion- 

3. Low  or  normal  .... 

ally  compensated  by  increased 
force  of  heart-beat  and  dimin- 
ished viscosity  of  blood. 
Blood-pressure  rises  on  account 
of  marked  increase  in  force  of 
heart-beat  in  spite  of  empty- 
ing of  vascular  system  and  of 
relaxation  of  peripheral  vessels. 

Quite  independently  of  these  changes  the  right  border  of  cardiac  dul- 
ness  recedes  one  or  more  centimetres  toward  the  sternum,  the  venous  pressure 
should  fall,  and  the  general  condition  should  improve  (cf.  Fig.  127  and  case  on  page  239). 

Contraindications  to  Venesection. — However,  it  must  be  borne  in  mind 
that  venesection  can  do  harm  as  well  as  good.  Gushing  has  shown  that  in 
conditions  with  increased  intracranial  tension,  among  them  apoplexy,  the 


*  Heubner  has  shown  that  two-thirds  of  the  viscosity  of  the  blood  is  due  to  the  cor- 
puscles, hence  venesection  cannot  fail  to  reduce  the  viscosity. 


TREATMENT   OF   FAILURE   OF   THE   HEART. 


167 


high  blood-pressure  is  a  phenomenon  of  physiological  compensation,  which 
is  necessary  in  order  to  maintain  the  circulation  through  the  medulla.  In 
conditions  with  long-continued  high  blood-pressure,  especially  chronic 
nephritis,  this  may  also  be  the  case.  In  these  conditions  venesection  with 
a  view  to  lowering  the  arterial 
pressure  is  contraindicated;  but 
in  these,  as  in  other  conditions, 
it  is  still  the  procedure  of  choice 
to  relieve  pulmonary  oedema  or 
acute  dilatation  of  the  right  heart. 
The  venesection  should  be  carried 
only  to  the  point  of  relieving  the 
venous  stasis,  not  to  that  of  low- 
ering the  arterial  pressure. 


DIET. 

Rest  for  the  gastro-intestinal 
tract  is  quite  as  important  for 
the  heart  as  is  rest  for  the  mus- 
cles. Erlanger  and  Hooker  have 
shown  that  "  an  increase  in  pulse- 
pressure  becomes  manifest  within 


Fig.  127. — Effect  of  venesection  on  the  cardiac  out- 
line, showing  diminution  in  size  of  right  heart.  (Case 
of  G.  G.)  SoUd  line  indicates  cardiac  outline  before 
venesection,  broken  line  after  venesection. 


BEFORE  VENESECTION     AFTER  VENESECTION 


a  few  minutes  after  the  beginning  of  the  meal,  reaches  its  maximum  within 
one  or  two  hours,  and,  as  a  rule,  declines  somewhat  more  slowly.  It  seems 
to  pass  off  within  one  or  two  hours  after  the  maximum  has  been  reached. 
The  pulse-rate  is  always  distinctly  increased  with  the  ingestion  of  meals. 

....  The  product  P.  P.  X 
P.  R.,  representing  the  velocity, 
follows  the  curve  of  the  pulse- 
pressure,"  hence  the  velocity 
of  flow  and  the  work  of  the 
heart  are  increased.  Accord- 
ingly, the  diet  should  be  light, 
just  enough  to  keep  the  patient 
nourished  without  ever  giving 
him  a  sense  of  fulness  or  to 
allow  gas  to  form  in  the  stom- 
ach and  intestines.  Distention 
of  the  stomach  pushes  up  the 
diaphragm  and  causes  the 
heart  to  lie  more  transversely 
in  the  thorax,  embarrassing 
its  action,  causing  a  diminution  in  the  systolic  output  and  an  increase 
in  the  pulse-rate.  Not  infrequently  this  is  also  associated  with  onset 
of  precordial  pain  and  constriction.  Accordingly  a  very  light  diet 
is  necessary  for  the  patient  suffering  from  heart  failure.  The  1  a  c  t  o  - 
cereal  diet  is  the  best,  consisting  mainly  of  milk,  eggs,  custards, 
junket,  toast,  zweiback,  crackers.     The  numerous  prepared  cereal  foods, 


Fig.  128. — Typical  effect  of  venesection  upon  the  circu- 
lation.   Arrows  indicate  change  in  blood-pressure. 


168  DISEASES   OF   THE   HEART    AND    AORTA. 

which  consist  of  partially  toasted  flakes  of  wheat,  corn,  or  rice,  are 
particularly  good,  since  much  nourishment  may  be  given  in  small  bulk 
and  in  a  form  which  does  not  tend  to  form  thick,  impenetrable,  doughy 
masses.  Besides  they  contain  the  bran  as  well  as  the  starch,  and  hence, 
by  leaving  considerable  fecal  residue,  tend  to  keep  the  bowels  moving.  Meat 
should  be  given  sparingly,  partly  because  the  purin  bodies  (xanthin,  hypo- 
xanthin)  tend  to  raise  the  blood-pressure  and  increase  the  work  of  the  heart, 
and  more  particularly  because  the  meat  fibres  are  relatively  slow  in  diges- 
tion. For  this  reason  it  is  better  to  take  the  proteid  food  in  the  forms  men- 
tioned above.  Finely  hashed  Hamburg  steak,  lamb  chops,  or  chicken  are 
the  best  forms  of  meat. 

Liquid  and  Salt. — Liquids  should  be  limited  to  1500  c.c.  (three 
pints)  a  day  in  cases  where  oedema  is  present,  since  an  excess  of  liquid 
ingested  causes  further  accumulation  of  oedema  as  well  as  bringing  on  a 
slight  overfilling  of  the  blood-vessels,  and  thereby  increasing  the  work  of 
the  heart. 

Salt  should  also  be  withheld  from  the  food  as  far  as  possible,  since 
Widal  and  Javal,  Strauss  and  Richter  have  shown  that  it  is  a  contributing 
factor  in  the  production  of  oedema,  and  Barie  reports  good  results  from  the 
diminution  of  NaCl  in  the  diet  in  diseases  of  the  circulation. 

Barie  recommends  the  following  articles  as  a  basis  for  a  diet  low  in 
sodium  chloride:  Type  I — Unsalted  bread  500  Gm.  (18  oz.),  raw  meat  400 
Gm.  (14  oz.),  butter  80  Gm.  (2^  oz.),  sugar  100  Gm.  (3^  oz.).  Type  II— Pota- 
toes 1000  Gm.  (32  oz.),  raw  meat  400  Gm.  (14  oz.),  butter  80  Gm.  (2J  oz.), 
sugar  150  Gm.  (5  oz.). 

Sample  Diet. — An  excellent  diet  for  severe  heart  cases,  which  may  at 
least  serve  as  a  basis  for  other  variations,  is  the  following,  slightly  modified 
from  that  used  for  cardiac  cases  in  the  wards  of  the  Johns  Hopkins  Hospital: 

8  A.M.  Cereal,  soft  egg,  toast,  coffee  200  Gm.  (vi  oz.). 
10  A.M.  Milk  200  c.c.  (vi  oz.),  soft  egg,  crackers. 

Dinner  (noon).  Soup,  chicken,  potatoes. 

4  P.M.  Milk  200  c.c.  (vi  oz.). 

Supper,  6  p.m.  Milk  200  c.c.  (vi  oz.),  soft  egg,  crackers,  prunes.^ 

9  P.M.  Milk  200  c.c.  (vi  oz.),  bread. 

Limited  Mi!l<  Diet.  —  In  cases  of  broken  compensation  with  extreme 
oedema  great  success  has  sometimes  been  attained  by  limiting  the  diet  to 
600  to  800  c.c.  of  milk  in  24  hours  (Carell,  Hoffmann,  Jacob  and  Hirsch- 
feld),  even  in  cases  in  which  all  other  therapeutic  measures  have  failed. 
Professor  Barker  has  occasionally  obtained  excellent  results  by  increasing 
the  proteid  intake  upon  this  diet  through  the  addition  of  nutrose  to  the 
milk.  However,  striking  results  with  this  method  are  by  no  means  the 
rule,  and  it  is  to  be  used  with  caution. 

Alcohol. — A  very  little  alcohol,  either  as  wine,  or  as  brandy  or  whiskey, 
may  be  allowed  to  persons  accustomed  to  its  use.     Beer  is  less  advisable, 

'  It  is  important  to  avoid  giving  stewed  fruits  which  contain  much  acid,  such  as  peaches 
and  apricots,  along  with  the  milk,  as  the  digestion  of  patients  with  broken  compensation 
is  very  easily  disturbed,  and  an  attack  of  vomiting  places  a  considerable  strain  on  the  heart. 


TREATMENT   OF   FAILURE   OF   THE   HEART.  169 

since  it  carries  with  it  large  quantities  of  liquid  and  often  disturbs  the 
digestion  as  well,  whereas,  wine,  whiskey,  or  brandy  in  small  quantities 
improves  it.  Against  this  is  balanced  the  deleterious  effect  of  alcohol  upon 
the  heart  muscle.  Large  quantities  tend  to  produce  fatty  degeneration  of 
the  latter.  Whether  small  quantities  have  any  such  effect  in  the  individual 
case  is  uncertain,  but  it  must  be  borne  in  mind  that  the  injured  organ  is 
much  more  susceptible  to  deleterious  influences  than  is  the  healthy  organ. 
It  is  a  safe  rule  that,  in  persons  not  already  addicted  to  its  use,  brandy  or 
whiskey  be  given  only  in  doses  which  serve  as  carminatives,  and  not  in 
doses  intended  for  stimulation.  Even  the  psychic  effect  may  often  be 
secured  as  well  by  small  doses  as  by  large  ones.  One  point  in  favor  of  alco- 
hol in  man  as  against  animal  experimentation  lies  in  the  fact  that  in  such 
persons  it  greatly  increases  the  sense  of  well  being  and  removes  psychic 
depression  and  worry.  The  latter  may  be  especially  straining  upon  the 
heart,  and  hence  every  effort  should  be  made  use  of  to  ward  it  off,  especially 
during  certain  crises;  but  it  should  be  borne  in  mind  that  the  patient  may 
easily  become  dependent  upon  the  drink  to  arouse  his  spirits  and  in  this 
state  more  harm  than  good  is  done.  The  greatest  judgment  should  be  used 
in  the  administration  of  alcohol  even  in  small  quantities,  and  it  should  even 
then  be  reserved  for  crises  when  the  stimulation  of  every  fibre  is  all-impor- 
tant. On  the  other  hand,  alcohol  should  never  be  withdrawn  suddenly  from 
persons  addicted  to  its  use,  since  this  procedure  often  precipitates  an  attack 
of  delirium  tremens,  but  moderate  doses  (whiskey  15  c.c.  or  ^  oz.  every 
four  hours)  should  be  given. 

Tea  and  Coffee. — Whether  tea  and  coffee  should  be  given  depends 
largely  upon  the  patient.  In  some  persons  these  cause  marked  general 
nervousness,  sleeplessness,  tremor,  and  even  palpitation  and  irregularity; 
others  have  established  a  tolerance  such  that  no  effect  at  all  is  produced. 
The  caffein  itself  is  an  excellent  cardiac  tonic  of  the  digitalis  order,  and 
where  its  effects  on  the  nervous  system  are  not  manifest  it  may  prove  an 
excellent  adjuvant  to  the  treatment.  (A  cup  of  coffee  or  of  strong  tea 
contains  about  0.1-0.2  Gm.,  L^  to  3  gr. ;  the  pharmacological  dose  of  pure 
caffein  being  0.05  to  0.25  Gm.)  As  a  rule  it  is  safer  to  remove  them  from 
diet,  but  in  this  as  in  all  other  rules  individual  exceptions  can  be  made. 

Tobacco  should  not  be  used  under  any  circumstances.  Besides  the 
nervous  symptoms,  it  produces  vasoconstriction,  and  often  irregularities, 
palpitation,  and  even  precordial  pain.  Hence  it  is  particularly 
to  be  avoided  in  cases  of  cardiac  disease. 

PURGATION. 

In  patients  with  cardiac  disease,  and  especially  in  those  with  broken 
compensation,  the  question  of  purgation  assumes  unusual  importance.  In 
these  patients  purgation  seems  to  have  a  threefold  beneficial  action:  first, 
by  eliminating  the  products  of  waste  and  putrefaction,  to  which  they  are 
particularly  sensitive;  secondly,  by  relieving  the  distention  of  the  bowels 
from  gas  which  tends  to  push  up  the  diaphragm  and  to  embarrass  the  heart 
by  placing  it  in  a  more  transverse  position;  and  thirdly,  by  removing  fluid 
from  the  body  through  the  bowels.     This  last  effect  is  probably  of  con- 


170  DISEASES   OF   THE   HEART   AND    AORTA. 

siderable  importance,  since  Askanasy,  Kast,  and  others  have  shown  that 
broken  compensation  is  accompanied  by  hydremic  plethora.  Hydrsemic 
plethora  causes  a  rise  in  venous  pressure  and  a  dilatation  of  the  heart  (Roy 
and  Adami,  Cameron),  thus  embarrassing  the  circulation.  Moreover,  in 
broken  systemic  compensation  the  venous  stasis  also  affects  the  kidneys 
and  diminishes  the  excretion  of  fluid,  so  that  the  bowel  becomes  an  impor- 
tant accessory  channel  of  elimination.  It  is  therefore  the  hydragogue 
purgatives  which  are  indicated  in  cardiac  failure  and  not  merely  the  pur- 
gatives which  increase  peristalsis. 

In  most  cases  the  best  method  of  procedure  is  to  start  movement  of  the 
bowels  with  calomel  in  either  large  single  doses  (0.3-0.6  Gm.,  grs.  v-x)  or  in 
small  divided  doses  (.006  Gm.,  gr.  j\  half-hourly).  The  dose  of  calomel 
should  always  be  accompanied  by  a  small  dose  of  bicarbonate  of  soda 
(0.3-0.6  Gm.,  gr.  v-x)  to  avoid  disturbing  the  digestion.  Still  more  certain 
purgation  is  obtained  by  giving  a  single  dose  of  calomel  and  rhubarb  in 
equal  quantities  (0.3  Gm.,  gr.  v),  given  at  night.  In  all  cases  the  calomel 
should  be  followed  by  a  saline  purgative  the  next  morning.  Epsom  salt 
or  some  aperient  water  is  preferable  to  Seidlitz  powders  or  effervescent 
citrate  of  magnesia,  partly  because  of  the  action  of  the  organic  acids  upon 
the  residium  of  calomel,  but  chiefly  because  the  carbonic  acid  in  the  drug 
distends  the  bowels  and  pushes  up  the  diaphragm,  thus  embarrassing  the 
action  of  the  heart.  However,  Epsom  salts  and  aperient  waters  sometimes 
cause  nausea,  and  in  such  cases  the  advantages  gained  from  the  mildness  of 
the  Seidlitz  powder  may  outweigh  its  deleterious  effects. 

After  constipation  has  been  overcome  purgation  with  salines  should  be 
continued  vigorously  until  the  oedema  has  completely  disappeared.  Just 
how  vigorously  this  purgation  should  be  maintained  is  a  matter  of  some 
dispute.  Some  clinicians,  who  regard  presence  of  fluid  as  the  most  dele- 
terious factor,  believe  that  the  best  results  are  obtained  with  ten  to  fifteen 
fluid  stools  in  twenty-four  hours,  with  the  elimination  of  two  or  three  litres 
by  the  bowel.  Most  observers,  however,  believe  that  the  beneficial  advan- 
tages of  such  extreme  purgation  are  more  than  counterbalanced  by  the 
strain  which  they  place  upon  the  patient,  not  only  by  disturbing  his  rest, 
but  also  by  causing  a  considerable  rise  of  both  arterial  and  venous  pressure 
with  each  movement  of  the  bowels.  Indeed,  each  effort  at  stool  constitutes 
a  typical  Valsalva's  experiment,  which,  as  has  been  seen  (Fig.  116,  p.  132),  is 
accompanied  by  tremendous  rises  in  blood-pressure  and  in  weakened  hearts 
by  acute  dilatation. 

Mr.  W.  E.  Dandy  has  shown  that  the  rise  of  arterial  pressure  during 
the  act  of  defecation  is  from  30  to  50  mm.  Hg,  and  Mr.  C.  C.  Cody  has  found 
a  corresponding  rise  in  the  venous  pressure.  These  observations  are  sup- 
ported by  the  fact  that  sudden  death  at  stool  is  by  no  means  uncommon  in 
cases  of  cardiac  disease,  especially  in  cases  of  aortic  insufficiency,  and 
occurs  even  when  the  movements  have  been  kept  soft  by  daily  purgation 
with  salts. 

In  this,  as  in  most  other  therapeutic  procedures,  extreme  measures 
are  to  be  avoided  and  treatment  should  be  directed  to  secure  a  few  easy 
bowel  movements  without  too  much  disturbance  to  the  patient.  In  many 
cases  one  or  two  compound  cathartic  pills  (colocynth,  jalap,  gamboge,  and 


TREATMENT   OF   FAILURE   OF  THE   HEART.  171 

calomel)  at  night  and  a  dose  of  Epsom  salts  or  aperient  water  in  the  morn- 
ing maintain  just  the  correct  number  and  quality  of  stools.  Compound 
jalap  or  compound  licorice  powders  are  also  useful  from  time  to  time.  In 
stubborn  cases  elaterium  or  a  drop  of  croton  oil  may  be  resorted  to,  but 
should  be  used  with  extreme  caution. 

On  the  other  hand,  cascara,  aloes,  strychnine,  belladonna,  castor  oil, 
phenolphthalein,  and  the  other  purgatives  which  purge  by  increasing  peris- 
talsis, are  of  less  value  in  the  stage  of  broken  compensation,  since  they  do 
not  deplete  the  portal  system  nor  relieve  the  hydrsemia,  though  they  are 
satisfactory  enough  when  compensation  has  been  reestablished. 

BIBLIOGRAPHY. 

General  Principles  in  the  Treatment  of  Cardiac  Diseases. 

Erlanger  and  Hooker.     Quoted  on  page  35. 

Winternitz  and  da  Silva.  Quoted  from  Buxbaum,  Lehrbueh  der  Hydrotherapie,  Leipz.,  1903. 

Widal,  F.,  and  Javal,  A.:  La  cure  de  dechloruration;  son  action  sur  I'oedeme,  sur  I'hydra- 

tation  et  sur  ralbuminurie  a  certaines  periodes  de  la  nephrite  epitheliale,  Bull,  et  mem. 

Soc.  Med.  d.  hop.  de  Par.,  1903,  3  s.,  xx,  733. 
Widal,  F.,  and  Lemierre:  Pathogenic  de  certaines  oedemes  brightiques;   action  du  chlorure 

de  sodium  ing^re,  ibid.,  1903,  3  ser.,  xx,  678. 
Widal,  F.:  Die  Kochsalzentziehungskur  in  der  Brightschen  Krankheit,  Verhand.  d.  Kong. 

f.  innere  Med.,  Wiesbaden,  1909,  xxvi,  43. 
Strauss,  H.:  Zur  Frage  der  Kochsalz  und  Fliissigkeitszufuhr  bei  Herz  und  Nierenkran- 

ken.,  Therap.  d.  Gegenwart,  Berl.-Wien,  1903,  N.  F.  v,  433;   Symposium  on  Thera- 
peutics, Med.  News,  N.  Y.,  1903,  Ixxxiii,  673;  also,  Die  Chlorentziehung  bei  Nieren- 

und  Herzwassersucht,  Verhandl.  d.  Kong.  f.  innere  Med.,  Wiesbaden,  1909,  xxvi,  91. 
Die  Chlorentziehung  bei  Nieren-  und  Herzwassersucht,  Verhandl.  d.  Kong.  f.  innere  Med., 

Wiesbaden,  1909,  xxvi,  91. 
Richter,  P.  F.:  Experimentelles  ueber  Nierenwassersucht,  Berl.  klin.  Wchnschr.,  1905, 

xlii,  384. 
Barie,  E.:  The  Dechloridation  Treatment  in  Diseases  of  the  Heart,  Internat.  Clin.,  Phila., 

1906,  16th  ser.,  i,  26.     Cf.  also  Symposium  in  Verhandl.  d.  Kong.  f.  innere  Med., 

Wiesb.,  1909,  xxvi. 
■Carell,  quoted  from  Romberg. 

Hoffmann,  F.  A.:  v.  Leyden's  Handbuch  der  Ernahrungs  therapie,  1898,  i,  579. 
Jacoby,  L.:  Ueber  die  Bedeutung  der  Karellkur  bei  der  Beseitigung  schwerer  Kreislauf- 

storungen  und  der  Behandlung  der  Fettsucht,  Muenchen.  med.  Wchnschr.,   1908, 

Iv,  839. 
Hirschfeid,  F.:  Die  Karell'sche  Milchkur  und  die  Unterernahrung  bei  Kompensations- 

storungen,  ibid.,   1908,  Iv,   1587 


V. 

THE  EFFECTS  OF  DRUGS  IN  CARDIAC  DISEASE. 

It  does  not  lie  within  the  scope  of  this  work  to  enter  into  a  detailed 
discussion  of  the  pharmacology  of  the  drugs  used.  The  reader  is  referred 
to  the  text-books  upon  this  subject,  especially — 

Cushny,  A.  R. :  A  Text-book  of  Pharmacology  and  Therapeutics,  Philadelphia  and 
New  York. 

SoUmann,  Torald  :  Text-book  of  Pharmacology. 

Hatcher,  R.  A.,  and  Wilbert,  M.:  The  Pharmacopoeia  and  the  Physician,  Chicago, 
1907  (published  by  the  American  Medical  Association). 

Heinz,  R.:  Handbuch  der  experimentallen  Pathologic  und  Pharmacologic,  Jena,  1905. 

However,  since  it  is  frequently  inconvenient  to  refer  to  such  books,  a  brief  summary 
of  the  action  of  each  drug  will  be  given  with  especial  regard  to  its  clinical  application. 

The  drugs  used  in  the  treatment  of  cardiac  disease  may  be  of  value 
through  their  action  on  the  following  systems: 

I.  Upon  the  Heart  Muscle — digitalis,  strophanthus,  strychnine,  squills,  caffeine. 
II.  Upon  the  Peripheral  Vessels — constrictors:   camphor,  strychnine,  adrenalin, 
ergot,  digitalis,  nicotine  (tobacco),  caffeine;  dilators:  amyl  nitrite,  nitroglycerin,  sodium 
nitrite,  erythrol  tetranitrate. 

1.  Acting  upon  the  Cardiac  Nerves. 

A.  Slowing  the  heart  through  stimulation  of  the  vagus:  aconite,  digitalis,  strophanthus, 
sometimes  strychnine  and  caffeine,  nicotine,  veratrum  viride,  muscarin,  very  large  doses  of 
potassium  salts,  bile  salts,  blood  in  jaundice. 

13.  Increasing  the  heart-rate  through  paralyzing  the  vagi:  atropine,  cocaine,  amyl  nitrite 
and  other  nitrites. 

C.  Increasing  rate  through  stimulation  of  accelerators:  adrenalin,  amyl  nitrite,  and 
other  nitrites. 

D.  Paralyzing  accelerators:   apocodein. 

2.  Diminishing  Venous  Pressure  and  Stasis  by  Depleting  Portal  System: 
purgative  series,  especially  calomel,  the  saline  and  the  vegetable  purgatives. 

3.  Drugs  which  Increase  the  Tonicity  of  the  Cardiac  Muscle  in  pharmaco- 
logical doses:  digitalis,  strophanthus,  strychnine,  amyl  nitrite,  nitroglycerin,  calcium 
chloride  (transitory  effect). 

4.  Drugs  which  Decrease  Tonicity:  potassium  salts,  chloroform,  formic  acid,  salt 
infusion,  ether,  adrenalin. 

Tonicity  is  practically  unaffected  by  small  doses  of  aconite,  though  slightly  diminished 
by  larger  ones. 

DIGITALIS. 

Foremost  among  the  drugs  used  in  treatment  of  circulatory  diseases 
are  the  preparations  of  digitalis,  introduced  into  medical  practice  by  Wither- 
ing in  1785.  He  says  of  it:  "In  the  year  1775  my  opinion  was  asked 
concerning  a  family  receipt  for  the  cure  of  the  dropsy.  I  was  told  that  it 
had  long  been  kept  a  secret  by  an  old  woman  in  Shropshire,  who  had  some- 
times made  cures  where  the  more  regular  practitioners  had  failed.  .  .  , 
The  medicine  was  composed  of  twenty  or  more  different  herbs,  but  it  was 
not  very  difficult  for  one  conversant  in  these  subjects  to  perceive  that 
172 


THE   EFFECTS   OF   DRUGS   IX   CARDIAC   DISEASE.        173 

the  active  herb  could  be  no  other  than  the  foxglove.  ...  I  soon  found 
the  foxglove  to  be  a  very  powerful  diuretic.  .  .  I  use  it  in  ascites, 
anasarca,  and  hydrops  pectoris."  He  then  cites  the  results  obtained  in 
the  treatment  of  over  100  cases,  many  of  which  would  be  worthy  of 
modern  therapeutics. 

Drugs  of  Digitalis  Series.' — Digitalis,  strophanthus,  apocynum,  convallaria  majalis, 
squill  (scilla),  erythrophloeine,  helleborein,  antiarin  (antiaris  toxicara). 

Digitalis  consists  of  the  dried  leaves  of  Digitalis  purpurea  collected  from  the  flower 
at  the  commencement  of  the  second  year's  growth.  It  should  not  be  kept  more  than  one 
year.^     Average  dose  pulv.  digitalis  =  0.05  Gm.  (1  grain). 

Preparations.  Dose. 

Gram.  English. 

Fluid  extractum  digitalis 0 .  05  ^  I 

Extractum  digitalis 0.01  gr.  1/5 

Infusum  digitalis 

(1.5%  digitalis +  10%  alcohol +  15%  cinnamon  water) 8.00  3   ii 

Tinctura  digitalis 1 .  00  "l  xv 

(10%  of  crude  digitalis  in  dil.  alcohol) 

A  very  satisfactory  form  for  administering  digitalis  and  a  purgative  at  once  is 
Addison's  (or  Niemayer's)  pill,  made  up  according  to  the  following  prescription: 

Pulvis  digitalis  I  ^.^ 0.6  gr.x 

Pulvis  sciUae  . .  j 

Hydrarg.  chloridi  mit 0.08  gr.  1  1/4 

M.  fiat  in  pil.  x  seu  capsnlas  x. 

Sig.    One  pill  every  three  hours. 

The  calomel  may  be  increased  to  gr.  x,  or  may  be  replaced  by  blue-mass  (massa 
hydrarg.)  or  gray  powder  (hydrargyrum  cum  creta)  in  capsules. 

The  efficacy  of  Addison's  pill  depends  upon  the  care  taken  to  secure  an  active  prepa- 
ration of  digitalis  in  making  it.  Moreover,  its  action  may  be  uncertain,  owing  to  the  fact 
that  a  certain  amount  of  digitalis  is  eliminated  with  the  stool  without  having  been  absorbed. 

Derivatives  of  Digitalis. — Digitoxin — the  most  active  substance  derived  from 
digitalis,  producing  all  the  digitalis  effects;  soluble  in  alcohol;  insoluble  in  water,  except 
in  the  presence  of  digitonin.  Prepared  in  soluble  form  with  digitonin  under  the  trade  name 
" Digalen "  (Cloetta) .    "Digalen,"  dose  1  c.c. 

Digitalin  (digitalinum  verum  Kiliani) — a  white  amorphous  glucoside,  less  toxic  than 
digitoxin  but  otherwise  resembling  it  in  physical  properties  and  pharmacological  action. 
Dose  2-6  mg.  (gr.  sV-rV)- 

Roughly,  digitoxin  is  six  times  more  potent  than  an  equal  weight  of  digitalinum 
verum  (Fraenkel). 

Digitalin  " German" — amorphous  powder,  soluble  in  water  and  alcohol;  a  mixture 
of  pure  digitalin,  digitalein,  and  digitonin.    Dose  2-6  mg.  (gr.  A-tV)- 

Digitalein  and  digitonin  are  other  somewhat  similar  substances  which  have  no  phar- 
macological action. 

Strophanthus — the  ripe  seeds  of  Strophanthus  Kombe.  Tinctura  strophanthi,  10 
per  cent,  of  the  drug  in  65  per  cent,  alcohol.    Dose  0.5  c.c.  (Ti\,viii). 

'  A  very  full  discussion  of  these  drugs  is  given  in  Cushny's  article. 

^It  is  most  difficult  to  obtain  a  preparation  of  digitalis  leaves  of  which  one  can  be 
certain,  and  upon  this  alone  the  result  of  the  whole  treatment  depends.  Owing  to  the  varia- 
tions in  leaves  it  is  best  to  obtain  preparations  from  manufacturing  chemists  who  have 
standardized  them  from  physiological  effects  upon  frogs  or  mammals.  (The  term  "frog 
unit,"  "Froscheinheit,"  refers  to  the  amoimt  of  drug  which  will  kill  an  average  frog, 
leaving  the  heart  in  systole;  cf.  also  Sowton  and  especially  Edmunds  and  Hale.) 
Edmunds  and  Hale  have  shown  that  in  frogs  the  drug  acts  chiefly  on  the  heart,  in  mam- 
mals largely  on  the  nervous  system. 


174  DISEASES   OF  THE   HEART    AND    AORTA. 

Derivative  and  Active  Principle. — Strophanthin — a  white  crystalline  glucoside  of  con- 
stant composition  and  action,  soluble  but  undergoing  decomposition  in  water.  Hence 
best  prescribed  in  dilute  alcohol: 

Strophanthin 0 .  01  gr.  1/5 

Alcohol  dil 1.50  5  v 

Sig.    Teaspoonful  p.  c.  in  half  glass  of  water. 

R.  A.  Hatcher  has  shown  recently  that  the  absorption  of  strophanthus  and  strophan- 
thin from  the  gastro-intestinal  tract  is  very  uncertain,  and  that  it  is  liable  to  set  in  suddenly 
after  tremendous  doses  have  been  given  without  effect.  Hence  these  drugs  should  be 
administered  intravenously  or  intramuscularly. 

For  intravenous  or  intramuscular  injections  strophanthin  (amorphous)  is  put  up  in 
small  sterile  phials  (Boehringer  &  Co.).  It  is  very  useful  for  the  physician  to  carry  a  few  of 
these  in  his  emergency  case. 

Strophanthin  (Thoms)  is  said  to  be  crystalline  and  is  a  more  stable  and  more  uni- 
form preparation.     It  acts  in  doses  of  i  to  J  mg.  (gr.  2^5  to  yjjj). 

EFFECT    OF    DIGITALIS    ON    THE    NORMAL   HEART. 

Fraenkel  and  Schwartz  and  also  Cloetta  have  shown  that  in  thera- 
peutic doses  digitalis  has  no  effect  upon  the  normal  heart,  either  in  affect- 
ing the  strength  of  the  beat  or  in  bringing  about  hypertrophy.  Neither 
has  it  any  effect  upon  the  perfectly  compensated,  undilated  heart  with  a 
valvular  lesion.  Its  chief  effects  are  seen  in  dilated  hearts  whose  myo- 
cardium still  retains  some  reserve  power.  In  the  severest  stages  of  cardio- 
sclerosis and  fatty  degeneration  it  may  stimulate  the  fibres  to  the  limit  of 
their  power,  and  thus  do  actual  harm,  and  even  hasten  the  end. 

ACTION    OF    DIGITALIS.  ' 

Digitalis  has  the  following  actions:  (1)  it  stimulates  the  vagus,  both 
centrally  and  peripherally,  brings  about  slowing  of  the  heart,  and  diminishes 
conductivity;  (2)  it  increases  the  irritability,  force  of  contraction,  and 
tonicity  of  the  cardiac  muscle  in  both  auricles  and  ventricles,  slightly 
diminishing  conductivity  by  direct  action  upon  the  cardiac  muscle  even 
in  atropinized  hearts ;  (3)  it  causes  the  peripheral  blood-vessels  to  constrict, 
thereby  raising  the  blood-pressure;  (4)  a  diuretic  action,  mainly  through 
increase  in  the  rate  of  general  blood  flow;  (5)  it  causes  a  constriction  of  the 
coronary  blood-vessels  and  diminished  flow  through  the  walls  of  the  heart. 

As  shown  by  Cushny,  the  action  of  digitalis  may  be  divided  into  three 
stages,  characterized  by  the  following  phenomena: 

I.  Therapeutic  Stage. — Slowing  of  entire  heart,  increase  of  blood-pres- 
sure, increase  of  systolic  output  and  of  cardiac  tonicity,  peripheral  vaso- 
constriction, dilatation  of  coronary  arteries,  slowing  of  conductivity. 

II.  Stage  of  Irregularity. — The  heart-rate  becomes  somewhat  accel- 
erated and  irregular.  Cushny  thinks  that  this  irregularity  is  due  to  the 
fact  that,  besides  following  impulses  from  the  auricles,  the  ventricle  begins 
to  beat  with  a  rhythm  of  its  own.  A  pararrthymia  thus  sets  in,  and 
the  two  independent  rhythms  occasionally  produce  interference  and  pro- 
longed pauses.  In  this  stage  the  blood  flow  becomes  slowed,  although 
the  output  of  individual  systoles  is  much  increased. 

III.  Stage  of  Incoordination. — Extreme  irregularity  of  both  auricles 
and  ventricles  has  now  set  in,  both  beating  independently  of  one  another 


THE   EFFECTS   OF   DRUGS   IN   CARDIAC   DISEASE.        175 

(absolute  heart-block) .    The  blood  flow  has  now  markedly  slowed  and  beats 
become  irregular  in  force  and  rhythm.    Death  sets  in. 

Action  of  Digitalis  on  the  Coronary  Arteries. — Another  effect  of  digitalis,  namely, 
marked  constriction  of  and  lessened  blood  flow  through  the  coronary  vessels,  has  been 
demonstrated  by  Oswald  Loeb  upon  the  excised  heart.  This  is  due  mainly  to  the  digi- 
toxin,  and  occurs  even  at  a  time  when  the  size  and  force  of  the  cardiac  contractions  are 
definitely  increased.  Although  Dr.  G.  S.  Bond  in  the  writer's  laboratory  has  been  unable 
to  obtain  any  such  change  in  flow  through  the  coronary  arteries  of  the  dog's  heart  in  situ 
after  administration  of  digitalis  and  strophanthus,  there  is  considerable  clinical  evidence 
that  digitalis  sometimes  does  distinct  harm  in  patients  whose 
myocardium  has  undergone  extensive  fatty  degeneration,  or 
cardiosclerosis,  or  whose  arteries  are  sclerotic.  Strophanthin  pro- 
duces the  same  effects  though  in  less  marked  degree. 

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Fig.  129. — Tracings  showing  the  action  of  digitalis  upon  the  dog's  blood -pressure.  (After  Cushny.) 
A,  normal;  B,  therapeutic  stage,  with  incre.ised  blood-pressure  and  moderate  slowing  of  the  pulse,  but 
quickened  blood-flow;  C,  excessive  inhibition,  causing  low  blood-pressure  and  slowed  circulation;  D,  still 
further  slowing,  with  slight  arrhythmia;  E,  third  stage,  irregularity  with  further  rise  of  blood-pressure 
from  excessive  vasoconstriction. 

Effect  on  the  Blood=pressure. — The  rise  of  blood-pressure  due 
to  digitalis  is  in  part  due  to  the  increased  force  and  out- 
put of  the  heart,  in  part  to  the  constriction  of  the  periph- 
eral and,  especially,  the  abdominal  blood-vessels.  The 
velocity  of  blood  flow  (as  shown  by  product  of  pulse-pressure  X  pulse- 
rate*)  is  usually  increased  when  this  effect  is  brought  about  (Fellner, 
Fraenkel).  Strophanthus  causes  less  vasoconstriction  than  digitalis,  and 
hence  usually  affects  the  minimal  pressure  less  than  the  maximal,  but 
increases  the  velocity  of  blood  flow  without  causing  so  great  a  strain  upon 
the  heart.  Unfortunately,  the  preparations  of  strophanthus  are  less 
reliable  for  continuous  action. 

Occasionally  it  is  found  that  both  digitalis  and  strophanthus  actually 
lower  the  maximal  blood-pressure.  This  occurs  especially 
in  the  cases  where  the  circulation  through  the  medullary  centres  is 
impaired   by   venous   stasis    or   arteriosclerosis,   or  failure   of   the   heart, 

'  Janeway  has  reported  cases  in  which  digitalis  produced  great  improvement  without 
increasing  P.  P.  x  P.  R.  Considering  the  error  which  may  be  involved  in  this  calculation,, 
such  exceptions  are  not  surprising  (see  page  24). 


176 


DISEASES   OF   THE   HEART    AND    AORTA. 


and  the  high  blood-pressure  is  merely  the  result  of  general  reflex  vaso- 
constriction from  the  ischaemia  of  the  centre  (high-pressure  stasis).  When 
the  force  of  the  heart  is  increased  and  the  blood  passing  through  the 
centre  is  better  aerated,  the  vasoconstrictor  influence  is  no  longer  exerted 
and  the  general  blood-pressure  then  falls. 

Effect  of  Digitalis  on  Tonicity.— Clinically  the  most  important 
action   of   digitalis    is    its    effect    upon    the    tonus   of    the 

cardiac  muscle,  in  preventing  and  in 
overcoming  dilatation,  and  it  is  in  dilated 
hearts  that  the  beneficial  action  of  digitalis 
is  most  pronounced.  Frangois-Franck  (1882) 
demonstrated  that  the  administration  of 
digitalis  did  away  with  the  transitory  func- 
tional tricuspid  insufficiency  which  resulted 
from  stimulation  of  the  vagus.  Cushny  and 
Cameron  have  shown  marked  increase  in 
tonicity,  as  shown  by  diminution  in  cardiac 
volume.  iMoreover,  Cloetta  has  demon- 
strated that  the  prolonged  administration 
of  digitalis  prevents  the  heart  from  dilating 
in  experimental  aortic  insufficiency  (posi- 
tive intraventricular  pressure  during  dias- 
tole). The  hearts  of  animals  which  have 
been  treated  with  digitalis  are  smaller  and 
stronger  than  those  which  have  not  been  so 
treated  (see  page  377).  Colbeck,  Gossage, 
and  others  have  also  emphasized  the  impor- 
tance of  this  effect  on  cardiac  tonus. 

CHOICE    OF    DIGITALIS    PREPAR.'VTION'S. 

The  first  question  arising  is,  What  form  of 
digitalis  to  administer?  Numerous  attempts  to  iso- 
late and  administer  the  purified  active  principle  of 
digitalis  have  demonstrated  that,  though  several  such 
substances  (digitalin,  digitoxin,  digitalein,  digitonin) 
have  been  used,  digitoxin  comes  closest  to  the  crude 
drug.  Unfortunately,  pure  digitoxin  is  insoluble  in 
water  and  in  the  tissue  juices,  but  becomes  soluble 
in  the  presence  of  digitonin.  The  mixture  of  the  two 
substances  known  as  "digalen"  (Cloetta)  or  "soluble 
digitoxin"  is  on  the  market,  and  is  widely  used,  especially  for  intravenous  injection,  when 
rapid  effects  are  desired.  Digitalin,  especially  the  so-called  "German"  digitalin,  has 
been  much  more  widely  used  than  digitoxin,  but,  as  is  also  Kiliani's  digitalinum  verum, 
is  far  less  certain  and  less  active. 

However,  the  recent  critical  studies  of  Albert  Fraenkel  have  demon- 
strated that  the  crude  digitalis  is  at  least  as  satisfactory  as  any  of  its  deriva- 
tives, provided  its  toxicity  (lethal  dose  for  a  frog)  has  been  determined 
and  the  therapeutic  dose  standardized  accordingly.  This  is  all  important, 
since  digitalis  leaves  from  different  sources  vary  greatly  in  their  content  of 
digitoxin,  digitalin,  etc.,  and  a  mere  knowledge  of  the  weight  of  powdered 
leaves,  which  is  all  that  is  necessary  for  the  pharmacopoeial  preparations, 


Fig.  130. — Variations  in  blood-pres- 
sure in  a  patient  under  the  influence  of 
digitalis  and  nitroglycerin.  MAX,  max- 
imal blood-pressure  ;  MIN ,  minimal 
blood  -  pressure  ;  PP,  pulse  -  pressure  ; 
P  P  X  P  R,  pulse  -  pressure  X  pulse- 
rate:  DISC.  DIGITALIS,  discontinue 
digitalis. 


THE   EFFECTS   OF  DRUGS   IN   CARDIAC   DISEASE.        177 

gives  no  idea  of  the  actual  potency  of  the  drug.  Fraenkel  also  found  little 
or  no  difference  between  digitoxin  and  crude  digitalis  as  regards  the  time 
at  which  their  effects  set  in,  both  becoming  manifest  in  twelve  to  twenty- 
four  hours  after  administration  by  mouth  or  intravenously.  The  absence 
of  immediate  effects  from  digitalis  preparations  may  be  obviated  by  the 
use  of  strophanthin  intravenously.  This  drug  acts  with  great  certainty 
and  its  action  usually  sets  in  within  less  than  half  an  hour,  so  that  it  is 
very  useful  in  cases  where  immediate  effects  are  desired.  Fraenkel  recom- 
mends a  single  dose  of  strophanthin  intravenously  to  be  followed  within 
twenty-four  hours  by  digitalis  by  mouth,  so  that  the  effect  of  the  latter 
may  begin  as  that  of  the  strophanthin  wears  off.  Of  course  if  the  patient 
has  recently  received  digitalis,  strophanthin  should  not  be  used  for  fear  of 
cumulative  effect. 


Vasoconstriction 


Vol.  Leg 


Seconds 


Fig.  131. — Effect  of  digitalis  on  cardiac  tonicity  in  the  dog.  (Experiment  by  Dr.  Cameron.)  Upper 
<5urve,  volume  of  the  hind  leg,  taken  with  a  plethysmograph,  showing  vasoconstriction;  second  curve, 
volume  of  the  ventricles;  lower  curve,  blood-pressure  taken  with  the  Huerthle  membrane  manometer. 
Time  in  seconds.  A  small  dose  of  tincture  of  digitalis  injected  into  the  jugular  vein  at  the  arrow.  The 
effect  upon  tonicity,  T  +  ,  outlasts  both  the  rise  in  blood-pressure  and  the  vasoconstriction. 


An  example  of  Fraenkel's  remarkable  therapeutic  effects  may  be  quoted  here: 

Patient,  aged  57,  male,  admitted  to  Strassburg  Hospital  November  17,  1905.  Had 
rheumatic  fever  in  1869  and  again  in  1886.  Palpitation  when  at  vv^ork,  and  occasional 
swelling  of  legs  since  1900.     Drinks  considerably. 

Present  Condition. — Considerable  cedema  of  legs,  thighs,  and  scrotum.  Moderate 
ascites.  Dulness  and  diminished  breath  sounds  over  right  base.  X-ray  shows  heart 
shadow  enlarged  to  left  and  right:  dynamic  dilatation  of  aorta.  Pulse  irregular,  104  per 
minute,  maximum  pressure  180.  Pulv.  folia  digitalis  0.1  Gm.  (IJ  gr.)  three  times  a  day 
brought  pulse  down  to  86  in  4  days,  to  76  in  6  days,  increasing  diuresis  from  2000  to  4500 
and  5800  respectively. 

Another  attack  of  pain  in  joints  on  December  1;  left  cHnic  "improved  "  on  December 
11.  Returned  January  25,  1906.  CEdema  as  before;  ascites  marked — abdomen  108  cm. 
in  circumference.  Liver  palpable  four  fingers'  breadth  below  costal  margin.  Spleen  pal- 
pable. Dulness  and  diminished  fremitus  over  base  of  right  lung.  Heart  dilated  more  than 
before;  impulse  not  palpable;  first  sound  at  apex  reduplicated;  second  accentuated,  espe- 
cially over  pulmonic  area.  Slight  gallop  rhythm.  Heart  action  rapid  and  regular.  Marked 
orthopnoea  and  very  distressing  cough.    Patient  has  had  no  sleep  for  several  nights. 

The  following  table  shows  the  effects  of  the  intravenous  administration  of  strophan- 
thin upon  his  blood-pressure,  urine  output,  and  symptoms.     The  product  of  pulse-pres- 
sure and  pulse-rate  furnishes  a  very  rough  index  of  the  velocity  of  blood-flow. 
12 


178 


DISEASES   OF   THE   HEART    AND    AORTA. 


Time. 


Jan.  27,  10.30. 

10.40. 

10.45. 

11.00. 
Jan.  28 


Jan.  31 . 
Feb.    1. 


Blood-pressure, 


Max.  ■  Min. 


268 
286 


206 
206 


Pulse. 


260 


156 


Pulse-pressure 
X  Pulse- rate. 


Urine  in 
24  hours. 


92  5640  1600 

84  7490 

1  mg.strophanthin  intravenously 
Diuresis  begins 


80 


7904 


6050 


Dyspnoea  increasing. 
Pulse  feels  larger. 


No  feeling  of  constric- 
tion.    Sleeps  well. 


(Edema  almost  disappeared. 

(Edema  completely  disappeared. 

Patient  makes  uninterrupted  recovery  with  no  further  medication. 


PRECAUTIONS    AND    METHODS    OF    ADMINISTRATION. 

Flavoring.  —  Gastric  disturbances,  such  as  nausea  and  v  o  m  - 
i't  i  n  g ,  occasionally  result  from  the  administration  of  digitalis  prepara- 
tions or  derivatives.  This  is  in  part  due  to  the  direct  irritating  action  upon 
the  gastric  mucous  membrane  and  in  part  to  the  extremely  unpleasant  taste 
and  after  taste  of  the  drug.  In  order  to  obviate  the  former  the  drug  should 
always  be  given  in  a  large  quantity  (at  least  half  a  tumbler)  of  water.  The 
intensely  disagreeable  taste  of  the  digitalis  and  strophanthus  preparations 
may  be  disguised  by  the  addition  of  bitter  orange  peel  (tinctura  aurantii 
amari),  compound  tincture  of  either  gentian  or  cardamom,  or  tincture  of 
quassia  or  calumba.  It  may  also  be  given  in  albumin  water  flavored 
with  lemon  so  that  its  taste  is  barely  noticeable.  The  use  of  any  of 
these  disguises  greatly  lessens  the  discomfort  of  the  patient  and  frequently 
minimizes  the  gastric  disturbances  resulting  from  the  drug. 

Rectal  Administration. — When  the  gastric  symptoms  persist  in  spite 
of  these  precautions,  the  drug  may  be  administered  per  rectum,  being  given 
in  100  c.c.  physiological  salt  solution  with  a  little  starch.  This  method  is 
very  satisfactory  (Janeway).  Dr.  Finley  informs  the  writer  that  he  has 
seen  the  pulse-rate  slowed  and  the  patient's  condition  greatly  improved 
within  two  hours  after  the  administration  of  digitalis  per  rectum^ 
whereas  the  effect  rarely  follows  administration  by  mouth  in  less  than 
twenty-four  hours. 

Period  of  Administration. — In  the  administration  of  digitalis  it  is  impor- 
tant to  obtain  a  definite  effect  and  yet  not  to  push  the  drug  beyond  the  first 
stage  of  its  activity, — that  of  slowing  and  increase  in  size  of  the  pulse, — and 
to  avoid  the  onset  of  the  second  stage,  i.e.,  of  irregularity.  Since  different 
hearts  vary  in  their  susceptibility  to  digitalis,  and  since,  on  the  other  hand, 
the  drug  begins  to  act  only  after  twenty-four  hours  and  may  have  a  cumula- 
tive effect,  this  task  is  by  no  means  easy.  To  avoid  the  onset  of  toxic  effects 
various  routine  methods  may  be  resorted  to.  Thus,  Professor  Osier  and 
other  authorities  recommend  giving  the  drug  in  "courses"  consisting  of 
eight  doses  of  15  minims  of  the  tincture  (0.1  Gm.  or  1^  gr.  digitalis)  every 
four  hours.  The  course  is  to  be  repeated  if  necessary.  It  may  be  said  that 
this  method  often  falls  short  of  the  effect  or  brings  it  about  too  slowly. 
The  writer  has  found  it  very  satisfactory  to  order  "0.3  c.c.  (5  minims)  of 


THE   EFFECTS   OF   DRUGS   IN   CARDIAC   DISEASE.        179 

the  fluidextract  three  times  a  day  until  the  pulse-rate  reaches  80,  when  it 
should  be  discontinued  without  the  necessity  of  a  special  order."  Albert 
Fraenkel  suggests  giving  several  strong  doses  equivalent  to  0.1  Gm.  (2  gr.) 
of  powdered  digitalis  (about  twice  the  usual  dose,  2  c.c.  or  30  minims  of 
the  tinctura  digitalis)  to  insure  prompt  effect  (slowing  of  the  pulse),  and 
thereafter  dropping  to  steady  dosage  of  .03  Gm.  (^  gr.,  0.5  c.c,  or  7^ 
minims  of  the  tincture)  to  prevent  cumulative  but  retain  the  therapeutic 
effect.  This  seems  to  be  the  most  satisfactory  method,  since  it  insures 
not  only  the  immediate  but  a  permament  effect.  Indeed  in  many  chrome 
cases  "  the  strength  of  the  heart  begins  to  fail  a  short  time  after  leaving  off 
the  digitalis.  Here  the  continuous  use  of  digitalis  (0.05  Gm.  or  1  gr.  digi- 
talis), as  recommended  by  Kussmaul,  Naunyn,  and  Groedcl,  for  months  and 
even  years,  has  an  admirable  effect  in  keeping  the  cardiac  activity  at  its 
necessary  height"  (Romberg).  . 

Digitalis  and  Nitrites.  —  In  many  cases  digitalis  and  nitro- 
glycerin, sodium  nitrite,  or  erythrol  tetranitrate  may 
be  given  together  with  great  advantage  (J.  O.  Hirschfelder).  This  com- 
bination of  drugs  does  more  than  merely  annihilate  the  constrictor  effect 
of  the  digitalis,  for  the  nitrites  also  increase  cardiac  tonicity  and  the  two 
drugs  unite  in  bringing  about  this  beneficial  effect.  Moreover,  it  is  a  well- 
known  principle  in  therapeutics  that  the  combined  effect  of  two  equivalent 
doses  of  drugs  having  a  common  action  is  often  greater  than  would  be  pro- 
duced by  using  double  the  dose  of  either  one.  As  will  be  seen,  this  combined 
action  is  particularly  important  in  the  treatment  of  aortic  insufficiency. 

ARRHYTHMIA    AND    HEART-BLOCK    CAUSED    BY    DIGITALIS. 

Mackenzie  and  later  Hewlett  have  investigated  the  nature  of  arrhyth- 
mias which  have  been  produced  clinically  by  slight  cumulative  action  of 
digitalis.    They  found  two  forms: 

First,  the  ventricle  occasionally  fails  to  respond  to  contractions  of  the  auricle  (par- 
tial heart-block).  V.  Tabora  has  found  in  animals  that  this  block  is  brought  about  mainly 
by  stimulation  of  the  vagi.  If  the  vagi  have  been  sectioned  or  paralyzed  with  atropine, 
it  appears  only  after  a  much  greater  dose  has  been  administered.  Hence  this  digitalis 
block  may  be  regarded  as  belonging  to  the  first  stage  of  digitalis  effect.  To  obviate  this, 
Hewlett  recommended  giving  atropine  along  with  the  digitalis,  a  combination  suggested  by 
Cushny  but  discarded  by  him  in  favor  of  digitalis  and  spartein,  a  drug  which  paralyzes  the 
vagus  without  the  unpleasant  action  of  atropine  (Cushny  and  Matthews).  Neither  of  these 
combinations  has  been  used  extensively,  and,  moreover,  Cameron's  experiments  show  that 
atropine  prevents  digitalis  from  improving  the  cardiac  tonicity,  and  hence  robs  it  of  its 
most  important  effect.  The  second  form  of  irregularity  following  digitalis  is  the  occurrence 
of  ventricular  extrasystoles,  such  as  were  observed  in  animals  by  Cushny.  As  stated  by 
this  observer,  this  effect  belongs  to  the  second  stage  of  digitalis  action,  and  accordingly  is 
a  more  urgent  sign  for  discontinuing  the  digitalis  than  is  even  the  partial  heart-block. 

ADMINISTRATION    OF    DIGITALIS    IN    WEAKENED    HEARTS. 

The  relation  of  digitalis  to  the  arrhythmias  has  recently  been  investi- 
gated by  Dmitrenko,  who  claims  that  drugs  of  this  series  are  always  con- 
traindicated  in  cases  where  the  heart  is  irregular.  This  is  certainly  an 
extreme  view.  Hering  has  shown  that  certain  irregularities,  due  to  extra- 
systoles  arising  in  the  ventricle,  disappear  under  the  use  of  digitalis.    Mac- 


180  DISEASES   OF  THE   HEART   AND    AORTA. 

kenzie  has  shown  that  where  the  irregularity  arises  in  the  auricle  digitalis 
may  sometimes  do  positive  harm  by  diminishing  conductivity;  but  this  is 
comparatively  rare.  On  the  other  hand,  da  Costa,  Leyden,  and  the  later 
writers  have  shown  that  in  the  permanent  irregularities  digitalis  does  not 
cause  the  arrhythmia  to  disappear,  but  usually  increases  the  force  of  the 
individual  contractions,  causes  them  to  become  less  unequal,  and  increases 
the  velocity  of  blood  flow.  The  effect  depends  largely  upon  the  condition 
of  the  heart  and  its  susceptibility  to  the  drug.  In  general,  the  more  diseased 
the  organ  the  more  sensitive  it  is  to  the  action  of  small  quantities.  A  very 
weak  heart  with  intense  myocardial  change  may  therefore  pass  to  the  second 
stage  of  digitalis  action  under  smaller  doses  than  would  bring  about  a 
physiological  effect  in  one  whose  fibres  were  less  intensely  degenerated. 
The  effect  of  digitalis  upon  the  patient  must  always  be  carefully  watched, 
and  if  the  rhythm  becomes  more  irregular  it  must  be  discontinued.  On 
the  other  hand,  where  the  myocardium  is  reduced  to  small  amount  in  ex- 
treme fatty  or  fibrous  myocarditis,  the  increased  strain  (and  perhaps  also 
the  coronary  vasoconstriction)  caused  by  digitalis  is  often  too  great,  and 
the  failure  of  the  heart  is  increased  and  the  drug  does  distinct  harm.  At 
present  no  absolute  rule  can  be  laid  down  for  the  border-line  cases  in  which 
there  is  doubt,  except  that  when  an  irregularity  is  present,  especially  one 
which  has  its  origin  in  the  auricle  or  great  veins,  digitalis  should  be  used 
only  to  treat  cardiac  dilatation,  and  even  then  with  great  hesitancy  and 
extreme  precaution.  When  any  disturbance  of  conductivity  occurs,  digi- 
talis is  absolutely  contraindicated. 

HALLUCINATIONS    FROM    DIGITALIS. 

Another  toxic  effect  of  digitalis  lies  in  the  production  of  mental  symp- 
toms, delirium  and  delusions,  through  its  action  on  the  central  nervous 
system  (Duroziez,  Hall,  see  page  160).  The  onset  of  these  symptoms 
therefore  constitutes  a  contraindication  to  continuing  the  drug. 

CHOICE    OF    DRUGS, 

As  between  digitalis  and  strophanthus,  the  choice  lies  with  the  former 
except  in  the  following  conditions:  (1)  when  rapid  action  is  needed,  in 
which  case  strophanthin  should  be  given  intravenously;  (2)  in  cases  of 
myocardial  weakness  or  fatty  degeneration,  when  it  is  important  not  to 
increase  peripheral  resistance;  (3)  in  cases  of  aortic  insufficiency  and  of 
mitral  stenosis,  where  the  same  is  true;  (4)  in  some  cases  with  aneurism  and 
broken  compensation. 

Besides  digitalis  and  strophanthus  numerous  other  drugs  and  their 
derivatives  enumerated  above  have  been  introduced,  but  none  seems  to 
have  any  decided  advantages  which  warrant  supplanting  these  two. 

SUMMARY    OF    CLINICAL    APPLICATION    OF    DIGITALIS. 

Professor  Osier's  epigram,  "  Broken  compensation  is  the  signal  for 
digitalis,"  about  summarizes  the  use  of  the  drug.  Its  applicability  in  indi- 
vidual diseases  will  be  discussed  under  the  separate  chapters,  but  in  general 


THE   EFFECTS   OF   DRUGS   IN   CARDIAC   DISEASE.       181 

it  may  be  said  to  be  useful  in  three  classes  of  conditions:  (1)  in  cases  where 
compensation  is  broken;  (2)  in  cases  where  acute  dilatation  is  present  and 
has  persisted  after  rest  and  other  modes  of  treatment;  (3)  in  cases  with 
persistent  or  distressing  tachycardia,  which  does  not  yield  to  other  means. 
It  is  in  general  absolutely  contraindicated:  (1)  in  cases  with  heart-block; 
(2)  where  the  amount  of  heart  muscle  has  been  diminished  by  fibrous  or 
fatty  myocarditic  changes,  or  in  a  case  in  which  digitalis  has  been  known 
to  fail  already.  It  should  be  used  with  caution:  (1)  in  arrhythmias  due  to 
disturbances  arising  in  the  auricles  or  sinus  region ;  strophanthus  is  equally 
contraindicated ;  (2)  in  cases  with  coronary  sclerosis,  owing  to  the  constrict- 
ing action  upon  those  vessels,  strophanthin  is  here  less  undesirable. 

STRYCHNINE. 

PREPARATIONS. 

Strychnine  (strychnina)  is  an  alkaloid  obtained  from  nux  vomica.  Tinctura  nucis 
vomicae  contains  2  per  cent,  extract  of  nux  vomica  and  is  assayed  to  contain  0.1  per  cent, 
strychnine.  It  is  useful  more  as  a  stomachic  bitters  than  as  a  cardiac  stimulant.  Dose, 
1-2  c.c,  15  to  30  minims. 

Strychninse  sulphas  contains  5  molecules  of  water  of  crystallization  and  78  per  cent, 
of  strychnine,  soluble  in  3  parts  of  water.     Average  dose,  0.0015  Gm.  (jV  gr.). 

Strychninse  nitras  is  soluble  in  42  parts  of  water  and  120  parts  alcohol.  Dose,  same 
as  sulphate. 

PHARMACOLOGICAL    ACTION    OF    STRYCHNINE. 

There  are  many  cases  in  which  the  circulation  is  beginning  to  show 
some  signs  of  slight  weakening  and  yet  where  it  does  not  seem  necessary 
to  use  digitalis.  In  these  cases  other  drugs  are  resorted  to, — in  America 
usually  strychnine,^  in  Germany  usually  camphor;  both  apparently  yielding 
good  clinical  results.  It  must  be  added,  however,  that  according  to  most 
pharmacologists  strychnine  has  no  effect  whatever  upon  the  heart  and 
produces  the  rise  in  blood-pressure  only  by  the  vasoconstrictor  action. 

Effect  on  Cardiac  Tonicity. — Dr.  P.  D.  Cameron  has  recently  investi- 
gated the  subject  under  the  writer's  direction,  and  has  found  in  the  dog 
that  strychnine  in  doses  of  .00003  Gm.  per  kg.  or  ^jVt  gr-  per  lb.,  corre- 
sponding to  002  Gm.  (^V  gr-)  hypodermically  for  a  man,  always  produces 
an  increase  in  tonicity  of  the  heart  muscle,  though  without  affecting  the 
force  of  the  beat  or  -markedly  changing  maximal  pressure.  Mean  and 
minimal  pressures  are  usually  slightly  increased  (by  10-15  mm.  Hg)  and 
pulse-rate  a  little  slowed.  Larger  doses  increase  the  systolic  output,  raise 
the  blood-pressure,  slow  the  heart,  and  increase  the  tonicity. 

Clinical  Effects. — In  view  of  the  wide-spread  and  often  indiscriminate 
use  of  this  drug,  it  is  important  to  realize  exactly  its  clinical  use  before 
prescribing  it.  As  has  been  stated,  strychnine  stimulates  both  vasocon- 
strictor and  vagus  centres,  hence  raises  the  blood-pressure  and  slows  the 
pulse-rate.  These  effects,  however,  have  been  observed  mainly  in  animals, 
and  few  exact  clinical  studies  have  been  made  upon  man  in  connection 

'  In  view  of  the  wide  use  of  strychnine  in  heart  diseases  in  English-speaking  countries, 
it  is  quite  striking  that  this  drug  is  not  mentioned  in  connection  with  therapy  of  the  cir- 
culatory system  in  such  extensive  German  text-books  as  those  of  Romberg  and  Heinz. 


182 


DISEASES   OF   THE    HEART    AND    AORTA. 


with  observations  of  the  change  of  blood-pressure.  Briggs  and  Cook,  who 
were  most  enthusiastic  over  the  use  of  the  drug,  did  not  obtain  rises  of 
blood-pressure  exceeding  10  mm.  Hg  from  doses  of  1  to  6  mg.  (-^\  to  yV  gr.) 
and  in  no  case  slowing  of  the  pulse.  Cabot  and  F.  P.  Drayer,  on  the  other 
hand,  failed  to  note  any  changes  whatever  in  many  cases.  The  writer  has 
made  a  considerable  number  of  observations,  determining  the  blood-press- 
ure with  the  Erlanger  apparatus.     He  injected  strychnine  in  doses  which 


Before 


Before 

After 

liffliMH 

1 

T    -T 

U      ,Illlll!l!llllllilllll!ll|!|        .llllllllllllllllllllllllliriilll :" 

I  II 

Fig.  132. — Curve  showing  the  effect  of  strychnine  upon  cardiac  tonicity.  (Experiment  by  Dr. 
Cameron.)  Lettering  as  in  Fig.  131.  Fig.  I  shows  increase  in  systolic  output  and  maximal  blood-pressure. 
Fig.  II  shows  increase  in  tonicity,  with  a  diminution  in  the  systolic  output  and  a  fall  in  the  minimal,  but  no 
change  in  the  maximal  blood-pressure.    The  effect  upon  tonicity  is  the  most  constant  effect  of  the  drug. 


rose  to  15  mg.  {\  gr.)  hypo,  without  obtaining  any  effect  upon  maximal 
or  minimal  pressure,  pulse-rate,  or  rate  of  respiration,  and  from  single 
doses  scarcely  any  increase  in  reflexes.  These  tests  were  made  upon  hearts 
which  were  not  dilated,  and  hence  no  effects  upon  tonicity  could  be  noted. 
Since  the  rank  and  file  of  English  and  American  phy.sicians  entertain 
an  almost  superstitious  belief  in  the  efficacy  of  this  drug,  it  is  evident  that 
effect  in  each  case  should  be  controlled  by  blood-pressure  determinations. 
Cameron's  experiments  upon  animals  have  shown  that  a  distinctly  bene- 


THE   EFFECTS   OF   DRUGS   IN   CARDIAC   DISEASE.        183 

ficial  effect  upon  tonicity  may  be  obtained  with  but  little  change  (5-10  mm.) 
in  the  maximal  blood-pressure,  but  that  often  when  these  changes  are 
very  slight  the  effect  may  be  much  more  distinctly  shown  by  a  rise  in 
the  mean  or  minimal  pressure.  Both  should  be  carefully  watched  in  cases 
in  which  strychnine  is  given,  and  the  dose  should  be  sufficient  to  be  effec- 
tive. If  no  effect  is  obtained  it  should  be  discarded  for  some  more  potent 
drug. 

INDICATIONS    FOR    STRYCHNINE. 

It  is  probable  that  strychnine  is  of  particular  value  in  the  disturbances 
of  respiration  following  extreme  heart  failure,  such  as  Cheyne-Stokes  breath- 
ing, cardiac  asthma,  etc-.,  as  claimed  by  Eyster;  and  in  such  cases  it  should 
be  given  whether  digitalis  is  being  administered  or  not. 

By  virtue  of  its  stimulating  action  upon  the  vasomotor  centre,  strych- 
nine is  particularly  indicated  in  cases  in  which  this  centre  is  beginning  to 
fail.  This  is  particularly  the  case  in  all  infectious  diseases,  in  many  cases 
of  neurasthenia,  in  mild  shock,  in  some  cases  of  anaemia,  asthenia,  and  in 
many  convalescents.  Strychnine  should  be  used  not  to  replace  digitalis, 
but  may  be  given  as  a  prophylactic  to  prevent  the  heart  muscle  from  wear- 
ing itself  out  upon  a  relaxed  vascular  system.  When  the  heart  muscle 
once  shows  signs  of  giving  way,  when  marked  cardiac  dilatation,  etc., 
have  set  in,  its  period  of  usefulness  is  over.  Small  doses  of  digitalis  will 
then  do  the  same  work  better  and  will  do  more.  It  is  also  valuable  when 
given  along  with  digitalis.  The  value  of  strychnine  again  becomes  mani- 
fest in  the  later  stages  of  heart  failure  through  its  action  as  a  stimulant 
for  the  respiratory  centre.  Eyster  believes  that  it  is  particularly  useful  in 
warding  off  Cheyne-Stokes  respiration  and  also  in  the  treatment  of  the 
latter.  It  is  probably  still  more  useful  in  cardiac  asthma,  more  as  a  pro- 
phylactic measure  in  maintaining  the  activity  of  the  respiratory  centre 
than  in  stopping  individual  attacks;  and  it  may  also  prove  of  value  in 
warding  off  the  distressing  dreams  that  result  from  mild  asphyxia  dur- 
ing sleep,  as  well  as  the  attacks  of  tachycardia  and  other  unpleasant  con- 
ditions which  may  occur  as  the  result  of  waking  "with  a  start"  (asphyxia 
during  sleep). 

CAMPHOR. 

Camphor  is  a  white  substance,  soluble  in  alcohol,  ether,  and  chloro- 
form, whose  structural  formula  is — 

CH2 CH CH2 


Average  dose  0.12  Gm.  (2  gr.),  best  given  as  linimentum  camphorse  (camphorated 
oil),  which  contains  20  per  cent,  of  camphor  dissolved  in  cotton-seed  oil.  Average  dose 
0.75  to  2.0  c.c.  (20  to  45  minims),  available  for  hypodermic  use  or  by  mouth. 

Spiritus  camphorse,  a  10  per  cent,  solution  of  camphor  in  alcohol.  Dose  1  c.c.  (15 
minims) . 


184  DISEASES   OF   THE    HEART   AND    AORTA. 

Camphor,  like  strychnine,  is  a  stimulant  to  the  vasomotor  centre, 
but,  according  to  Cameron,  does  not  seem  to  have  so  pronounced  an  effect  on  tonic- 
ity. Like  strychnine  it  also  varies  in  its  effects  on  different  individuals.  Some  persons 
require  doses  twenty  times  as  large  as  do  others  before  an  effect  sets  in,  especially  when 
the  drug  is  given  by  mouth.  Camphor  is  most  important  for  its  use  in  shock.  It  is  given 
deeply  into  the  muscles  in  order  to  avoid  subsequent  inflammations.  It  is  not  so  valuable 
for  continuous  use.  As  recently  shown  by  Winterberg,  Seligmann,  and  Gottlieb  and 
Magnus,  camphor  has  also  a  very  distinct  action  upon  the  heart  muscle,  causing  the  fibril- 
lating  excised  heart  to  revive  from  fibrillary  contractions.  After  camphor  has  been  ad- 
ministered to  a  dog  the  ventricle  {in  situ)  can  be  thrown  into  fibrillary  contractions  by 
weak  faradic  stimuli  and  yet  recover.  On  the  other  hand,  a  direct  therapeutic  effect  upon 
the  heart  muscle  in  man  has  not  yet  been  proved. 

CALCIUM    SALTS. 

Calcium  chloride  and  other  salts  of  calcium  have  been  recommended  recently  as 
cardiac  stimulants  by  Lauder  Brunton  and  other  English  clinicians.  Although  the  action 
of  calcium  upon  the  excised  heart  is  indisputable,  its  effect  upon  the  heart  in  situ  has  been 
supposed  to  be  too  transitory  to  be  of  practical  value.  The  writer  has  been  unable  to  find 
any  effect  upon  the  maximal  and  minimal  blood-pressures  and  pulse-rates  of  a  number  of 
cases  of  typhoid  fever  who  were  receiving  calcium  lactate  in  sufficiently  large  doses  to 
hasten  coagulation.  Sladen  also  found  in  a  large  variety  of  cases  that  calcium  lactate  had 
no  effect  upon  pulse-rate  or  blood-pressure.  On  the  other  hand,  in  animals  calcium  chloride 
has  an  effect,  especially  upon  tonicity,  which  closely  simulates  that  of  strychnine.  Injec- 
tion of  considerable  quantities  directly  into  the  cavities  of  the  heart  revives  that  organ  as 
nothing  else  appears  to  do.  The  writer  has  found  that  in  some  cases  dogs'  hearts  that  had 
actually  stopped  beating  and  even  lost  their  mechanical  irritability  revived  to  such  an 
extent  as  to  resume  a  regular  rhythm  with  a  moderately  high  blood-pressure.  The  matter 
is,  however,  still  in  the  experimental  stage. 

CAFFEINE. 

From  the  results  of  experiments  upon  animals,  caffeine  would  take 
rank  next  to  digitalis  in  cardiac  therapy.  Like  digitalis  it  acts  upon  the 
cardiac  muscle,  increasing  the  size  and  force  of  the  contraction;  like  digi- 
talis it  has  a  vasoconstrictor  action,  and  raises  the  blood-pressure  by  bring- 
ing about  constriction  of  the  peripheral  blood-vessels.  It  is  therefore  par- 
ticularly valuable  in  conditions  of  collapse  and  shock.  In  this  regard  it  is 
more  reliable  than  camphor  (Romberg)  or  strychnine. 

On  the  other  hand,  caffeine  does  not  exert  a  constricting  action  upon  the  coronary 
arteries  (O.  Loeb),  and  hence  is  not  contraindicated  in  cases  of  coronary  sclerosis.  Upon 
the  pulse-rate  caffeine  exerts  a  variable  effect,  in  relatively  small  doses  (0.1  Gm.,  2  gr.) 
slowing  the  pulse  by  stimulating  the  vagi,  in  larger  doses  accelerating.  The  acceleration 
is  apparently  due  to  direct  action  upon  the  heart  muscle,  since  it  occurs  also  in  the  excised 
heart  when  caffeine  is  added  to  the  Locke's  solution.  However,  as  regards  the  effects  of 
a  given  dose,  there  is  the  greatest  variation  among  different  individuals,  some  persons 
being  extremely  sensitive  to  small  doses,  others  extremely  resistant.  Even  in  the  same 
individual  tolerance  varies.  Thus  a  considerable  degree  of  tolerance  may  be  developed  by 
the  constant  use  of  coffee,  so  that  three  or  four  cups  (0.15  to  0.2  Gm.,  3  to  5  gr.  caffeine) 
a  day  may  be  taken  with  no  symptoms  whatever.  Thus,  in  a  case  under  the  writer's  ob- 
servation, after  several  months  of  absolute  abstinence  from  coffee,  marked  palpitation, 
tachycardia,  and  sleeplessness  resulted  from  a  single  cup  in  twenty-four  hours;  a  few  weeks 
later  one  cup  and  after  a  few  months  two  cups  could  be  taken  without  any  apparent  effect. 

Unfortunately,  the  therapeutic  use  of  caffeine  is  often  accompanied  by 
palpitation,  sleeplessness,  and  even  nausea,  vomiting,  vertigo,  and  delirium, 
which  occur  with  particular  ease  in  cases  with  cardiac  disease.     In  using 


THE   EFFECTS   OF   DRUGS   IN   CARDIAC   DISEASE.       185 

caffeine  one  is  therefore  usually  in  a  dilemma  between  a  hypersensitiveness 
and  an  habituation.  Unfortunately,  the  palpitation  and  discomfort  usually 
set  in  at  about  the  same  point  as  the  therapeutic  effect,  or  even  earlier; 
but  there  are  certainly  many  cases  in  which  this  is  not  the  case,  and  in 
which  caffeine  is  a  valuable  therapeutic  agent. 

THEOBROMINE. 

Theobromine  has  a  much  less  effect  upon  the  cerebral  cortex  and  upon 
the  vasomotor  centre  than  caffeine,  but  has  a  very  strong  diuretic  action. 
As  shown  by  O.  Loeb  it  possesses  a  much  more  powerful  action  in  dilating 
the  coronary  arteries  of  the  excised  heart.  Upon  the  heart  in  situ  its  action 
does  not  seem  to  be  pronounced.  Indeed,  G.  S.  Bond,  in  the  writer's 
laboratory,  has  been  unable  to  detect  any  effect  upon  the  outflow  from  the 
coronary  veins  as  the  result  of  intravenous  injection  of  agurin  (theobromine 
sodium  acetate).  The  stimulating  action  of  theobromine  upon  the  heart 
muscle,  though  not  as  intense  as  that  of  caffeine,  is  still  very  marked.  It 
has  therefore  been  recommended  as  a  cardiac  stimulant,  particularly  by 
the  French  clinicians,  who  found  it  of  considerable  value  in  the  weak 
hearts  of  fatty  individuals.  Kaufmann  and  Pauli,  Brewer  and  v.  Leyden 
recommended  the  use  of  theobromine  in  attacks  of  angina 
pectoris  (stenocardia).  Pineles  advises  theophyllin.  Pal  has 
found  that  theobromine  is  occasionally  useful  in  the  treatment  of  vaso- 
motor crises,  but  that  it  often  fails  in  cases  where  iodine  and  potassium 
thiocyanate  help.  Romberg  is  not  able  to  detect  any  beneficial  action  of 
theobromine  apart  from  its  diuretic  action.  In  using  theobromine  it  is 
preferable  to  use  those  compounds  which  are  free  from  salicylates,  since 
this  radical  has  a  certain  depressant  action  upon  the  heart  and  an  irritant 
action  on  the  kidneys.  Acettheobromine  sodium  ("agurin")  and 
acettheocin  sodium  are  therefore  preferable  to  theobromine  sodium  sali- 
cylate C '  diuretin  ") . 

ACONITE. 

PREPARATIONS. 

A  c  o  n  i  t  u  m  ,  the  dried  tuberous  root  of  aconitum  napellus,  collected  in  autumn, 
and  yielding  not  less  than  0.5  per  cent,  aconitin.    Dose  0.05  Gm.  (1  gr.). 

Tinctura  aconiti,  U.S.  P.,  now  represents  10  per  cent,  of  the  crude  drug, 
formerly  stronger.  It  is  the  most  certain  and  most  stable  of  all  the  aconite  preparations. 
Dose  0.6  c.c.  (10  minims). 

Aconitina,  the  crystalline  alkaloid.  Dose  0.00015  Gm.  (0.15  mg.  or  iijogr.). 
It  is  so  irritating  that  it  is  usually  preferable  to  prescribe  the  simple  tincture  of  aconite, 
since  this  is  assayed  according  to  the  last  pharmacopoeia. 

Pharmacological  Action. — Aconite  has  three  pharmacological  actions 
upon  the  circulatory  system:  (1)  it  stimulates  the  vagus  promptly  and  to 
a  high  degree;  (2)  it  diminishes  the  size  and  force  of  the  cardiac  contrac- 
tion, and  also  accelerates  the  heart  when  this  organ  is  liberated  from  the 
action  of  the  vagus  centre;  (3)  it  slightly  stimulates  the  vasomotor  centre 
in  very  small  doses.  However,  it  also  diminishes  the  activity  of  the  respira- 
tory centre,  and  may  thus  bring  on  dyspnoea. 

Therapeutic  Uses. — When  carefully  given  in  therapeutic  doses  aconite 
slows  the  heart  by  stimulation  of  the  vagus,  and  has  little  action  upon  the 


18G  DISEASES   OF   THE   HEART    AND    AORTA. 

heart  muscle.  It  is  therefore  of  value  in  the  acceleration  of  the  pulse  in 
fevers,  where  the  heart  muscle  itself  needs  no  stimulation  and  the  heart 
needs  slowing.  Owing  to  the  variability  of  the  tincture  under  the  old 
pharmacopoeia,  the  use  of  aconite  has  fallen  into  disrepute,  and  enough 
time  has  not  elapsed  since  the  adoption  of  the  last  pharmacopoeia  (1900, 
adopted  in  1905)  for  its  real  utility  in  physiological  therapeutics  to  have 
been  investigated.  There  is  no  doubt  that  it  is  of  value  in  many  cases  of 
tachycardia,  especially  those  of  nervous  or  postfebrile  origin.  Da  Costa,  in 
1864,  found  it  of  some  value  for  the  tachycardia  of  acutely  overstrained 
hearts,  but  particularly  useful  when  given  with  digitalis. 
This  combination  contains  two  drugs;  both  stimulate  the  vagi,  the  one 
tends  to  diminish,  the  other  to  increase  the  force  of  cardiac  contraction.  If 
the  latter  effects  balance  each  other  it  may  be  possible  to  obtain  in  this 
way  the  purest  and  most  intense  action  in  slowing  of  the  pulse. 

It  is  certain  that  the  simultaneous  use  of  two  drugs  having  certain  actions  in  common 
often  brings  about  an  effect  not  obtainable  with  either  drug  alone;  but  since  the  reaction 
against  the  polypharmacy  that  reigned  during  the  middle  of  the  last  century,  the  tend- 
ency has  been  toward  the  use  of  single  drugs.  There  is  no  doubt  that  much  can  be  learned 
in  the  treatment  of  cardiac  diseases  by  judicious  combinations  along  the  lines  mapped  out 
by  pharmacological  experiments,  just  as  is  now  found  with  hypnotics,  analgesics,  and 
purgatives.  This  is  radically  different  from  the  ancient  polypharmacy,  in  which  hetero- 
geneous drugs  were  mixed  without  regard  to  their  action  or  antagonism. 

ADRENALIN. 

Adrenalin  (suprarenin,  epinephrin) ,  the  active  principle  of  the 
suprarenal  gland,  is  also  used  occasionally  to  raise  blood-pressure  by  its 
constricting  action  upon  the  peripheral  blood-vessels  and  slight  stimulating 
action  upon  the  heart,  but  its  action  lasts  only  from  one  to  two  minutes 
and  hence  it  is  of  little  value,  except  to  tide  over  a  sudden  failure  until 
some  other  drug  can  become  active. 

ERGOT. 

Ergot  has  been  recommended  by  some  writers  for  its  vasoconstrictor 
action  exerted  through  stimulation  of  the  vasomotor  centre.  It  also  stimu- 
lates the  vagal  centre.  Cronyn  and  Henderson  have  found  that  these  effects 
are  very  uncertain  when  the  drug  is  given  by  mouth,  but  occur  quite  uni- 
formly when  it  is  given  intravenously.  Since  this  is  rarely  necessary,  the 
use  of  ergot  may  be  confined  to  patients  with  vasomotor  failure,  in  which, 
like  adrenalin,  it  is  used  as  a  last  resort. 

NITRITES  AND  NITROGLYCERIN. 

PREPARATIONS.      (PHARMACOPCEIAL,  U.  S.  P.) 

Amyl  nitrite  (amylis  nitris),  a  liquid  containing  about  80  per  cent,  of  amyl  nitrite. 
Average  dose  0.2  c.c,  3  minims  (inhaled).  Usually  to  be  had  in  pearls,  each  pearl  contain- 
ing one  dose. 

Nitroglycerin  CH^ONOj 

1 
CHONO3 

I 
CH,ONO, 


THE   EFFECTS   OF   DRUGS   IX   CARDIAC   DISEASE.       187 

is  sold  in  tablets  of  varjing  size,  usually  one  tablet  containing  j^^  gr.  (0.6  mg.).  How- 
ever, in  tablet  form  the  nitroglycerin  is  liable  to  undergo  more  or  less  rapid  deterioration, 
and  hence  administration  in  this  form  is  unreliable.  It  is  best  given  as  spiritus  glycerylis 
nitratis  (spiritus  glonoini),  a  1  per  cent,  solution  of  nitroglycerin  in  alcohol,  which  should 
be  freshly  prepared  from  a  10  per  cent,  stock  solution.  Initial  dose  0.05  c.c.  (1  minim), 
increasing  if  necessary  1  minim  at  a  time. 

Sodii  nitris  (sodium  nitrite),  NaNOj,  a  white  fused  mass,  very  deliquescent  and 
slowly  becoming  oxidized  to  sodium  nitrate  on  exposure  to  the  air,  thus  becoming 
useless.    Dose  0.06-0.12  Gm.  (gr.  i-ii). 

There  are  also  several  non-pharmacopoeial  nitrates  which  are  very 
satisfactory.  Erythrol  tetranitrate,  CHjONOj-CHONOj-CHONOj- 
CHjONOj,  has  about  the  same  action  as  nitroglycerin,  except  that  it  acts 
more  slowly  (action  lasting  three  to  four  hours) .  Sold  as  tablets,  each  con- 
taining .03  Gm.  (^  gr.).  Dose  one  or  two  tablets  every  four  to  six  hours. 
In  the  cases  in  which  the  writer  has  used  it  erythrol  tetranitrate  has  been 
very  efficient  and  satisfactory. 

ACTION    OF    THE    NITRITES. 

In  practical  therapy  the  nitrites  are  drugs  of  great  importance.  In 
animals  they  are  found  to  act  upon  the  muscles  and  nerves  of  the  blood- 
vessels to  bring  about  an  intense  vasodilatation,  thereby  diminishing  the 
resistance  to  blood  flow  and  lessening  the  resistance  to  the  action  of  the 
heart.  As  far  as  can  be  judged  from  the  studies  of  O.  Loeb,  they  do  not 
influence  the  vasoconstrictors  of  the  coronary  arteries  unless  present  in 
concentration  which  is  absolutely  toxic 

to  heart  muscle.     G.  S.  Bond  has  found    .  w      min.  hours 

that  the  outflow  through  the  coronary 
veins  of  normal  dogs  is  decreased  rather 
than  increased  by  nitroglycerin  and 
amyl  nitrite.  It  is  therefore  question- 
able whether  these  drugs  ever  bring 
about  dilatation  of  the  coronary  arte- 
ries, as  has  been  supposed  from  their  Fig.  133.— Effects  of  drugs  of  the  nitrite 
Affipflpv  in  nno-inn  r»pptr>ric!  series  upon  the  blood-pressure  in  man.  (Schema 
emcacy    m    angina    pectoris.^               ^                       representing  the  findings  of  Hewlett  and  Mat- 

The  relation  of  the  various  nitrites     thews.)    mix,  minutes. 
to    one    another   as    regards    rapidity 

of  action  is  shown  in  Fig.  133.  The  effect  of  amyl  nitrite  sets  in  within 
a  minute  and  passes  off  within  five  minutes;  that  of  nitroglycerin  lasts 
from  about  the  seventh  to  the  twentieth  minute  after  administration, 
sodium  nitrite  from  the  fifteenth  to  the  thirty-fifth,  while  erythrol  tetrani- 
trate begins  to  exert  an  effect  only  after  about  fifteen  to  thirty  minutes, 
but  this  continues  for  three  to  four  hours. 

Amyl  Nitrite. — Hewlett  has  recently  made  a  careful  clinical  study  of  the  effects  of 
amyl  nitrite  inhalation,  and  found,  (1)  an  immediate  fall  of  maximal  pres- 
sure, average  13  mm.  Hg,  lasting  less  than  forty  seconds,  and  accompanied  by  a  less 
fall  of  minimal  pressure  and  an  increase  of  pulse-rate.  This  is  followed  by  a  second- 
ary rise  (about  28  mm.)  of  maximal  pressure  to  considerably  above  the  original  height, 
accompanied  by  a  less  marked  rise  of  the  minimal  pressure  and  by  a  return  of  pulse-rate 
to  the  normal.  These  changes  in  blood-pressure  correspond  to  an  increased  sys- 
tolic output  and  increased  force  of  heart-beat  (augmentor  effect) ,  and  Hewlett  was 
able  to  see  with  the  fluoroscope  that,  "as  the  action  of  the  heart  slowed  down  the  excur- 


188 


DISEASES   OF   THE   HEART    AND    AORTA. 


sions  of  the  left  ventricle  became  wider  by  one-half  centimetre,  but  they  soon  returned  to 
normal."  In  other  words,  besides  being  a  vasodilator  amyl  nitrite  is  a  very 
active  cardiac  stimulant,  more  rapid  than  any  except  adrenalin.  These 
findings  accord  well  with  the  results  of  Cameron  on  dogs,  that  nitroglycerin  both 
increases  cardiac  output  and  cardiac  tonicity  to  a  marked  degree. 
Relaxation  of  the  peripheral  blood-vessels  under  the  influence  of  the  amyl  nitrite,  as  shown 
by  the  plethysmograph,  was  present  throughout  all  Hewlett's  experiments  in  spite  of  the 
pecuhar  variations  of  blood-pressure.  The  vasodilatation  reaches  its  maximum  within 
the  first  minute  and  very  gradually  subsides  after  the  second,  but  a  definite  effect  is  still 
noticeable  ten  or  twelve  minutes  after.  In  older  persons  Hewlett  found  that  the  pulse- 
rate  often  did  not  change,  probably  owing  to  the  absence  of  the  tonic  activity  of  the  vagus. 

The  following  represent  typical  effects  in  normal  men  as  obtained  in 
the  very  careful  clinical  investigations  of  Hewlett  and  Matthew. 


Dose. 


Time  when 
action  begins. 


Amyl  nitrite  (Hewlett) 

Nitroglycerin  .05-.1  c.c.  (gr.  i-ij) 

Sodium  or  potassium  nitrate  .15  Gm.  (gr.  ij) .  . 
Erythrol  tetranitrate  .0.^.06  Gm.  (gr.  H)  •  •  • 
Manitol  tetranitrate  .06  Gm.  (gr.  i) 


15  sec. 
1  min. 
5  min. 
5h  min. 
12 


Maximal 

fall 
occurs  in 


Duration. 


1  min. 
4^  min. 
14  min. 
22  min. 
100  min. 


10  min. 
ihr. 


Nitroglycerin. — As  to  nitroglycerin,  there  is  tremendous  variation  in  its  effects  upon 
different  individuals,  A.  Loeb  having  reported  a  case  of  collapse  after  0.6  mg.  (xto  gr.), 
whereas  J.  Stewart  has  given  20  grains  a  day  to  a  single  patient. 

In  some  cases  it  is  impossible  to  obtain  a  fall  of  pressure  with  any  ordinary  doses. 
The  writer's  experience  agrees  with  that  of  Matthew,  that  the  effects  are  often  lacking  in 
cases  of  nephritis  in  which  high  blood-pressure  has  persisted  for  some  time.  To  this  might 
also  be  added  a  certain  group  of  arteriosclerotics  in  which  the  renal  symptoms  do  not  pre- 
dominate, although  it  is  possible  that  arteriosclerotic  changes  may  be  present  in  the  kidney. 

In  Prof.  J.  O.  Hirschf elder's  wards  it  was  customary  to  begin  with  a 
dose  of  1  gtt.  (sV  c.c,  i  minim)  every  half  hour,  increasing  1  gtt.  at  every 
third  dose  until  palpitation,  headache,  or  buzzing  in  the  ears  warned  that 
the  physiological  limit  had  been  reached.  The  next  dose  was  then  omitted 
and  a  permanent  dosage  of  1  gtt.  less  than  the  dose  last  given  was  then 
kept  up.  In  some  cases  as  much  as  1  c.c.  (15  minims)  of  the  1  per  cent, 
solution  was  given  every  half  hour  with  only  the  mildest  subjective  symp- 
toms, the  average  permanent  dose  being  0.3  to  0.6  c.c.  (5  to  10  minims). 
The  effect  of  these  doses  is  very  variable. 

Effect  on  the  Circulation. — A  fall  in  minimal  blood-pressure  is  the 
most  constant,  usually  accompanied  by  a  rise  in  pulse-pressure,  and  the 
maximal  pressure  sometimes  rising,  sometimes  falHng.  Hewlett  thinks  that 
there  is  combined  dilatation  of  the  blood-vessels  and  increased  systolic  out- 
put of  the  heart.  In  a  series  of  observations  upon  the  fluctuations  of  blood- 
pressure  after  the  administration  of  these  drugs,  made  with  the  Erlanger 
apparatus  independently  of  and  some  years  before  those  of  Hewlett,  the 
writer  had  noticed  effects  quite  similar  to  those  above  mentioned.  There 
seems  no  doubt,  therefore,  that,  as  stated  by  Hewlett,  the  beneficial  effects 
of  the  nitrites  in  man  are  due  to  something  more  than  a  simple  vasodilata- 
tion, and  indeed  it  is  possible  that  the  latter  may  play  often  even  a  minor 


THE  EFFECTS   OF   DRUGS   IN   CARDIAC   DISEASE.        189 

Tole.  Certain  it  is  that  in  many  cases  they  are  ideal  drugs  to  relieve  the  work 
of  the  heart  over  short  periods  when  the  blood-pressure  is  not  already  too 
low  to  admit  of  their  use.  However,  it  must  be  borne  in  mind  that  indi- 
vidual susceptibilities  vary,  and  the  patient  should  be  tested  with  amyl 
nitrite,  whose  effects  can  be  controlled,  before  any  other  nitrite  should  be 
given.  When  used  over  long  periods  of  time,  moreover,  the  production 
of  methsemoglobin  in  the  blood  may  be  brought  on  (shown  by  the  spectro- 
scope, or  by  a  chocolate  tint  in  the  blood),  which  is  distinctly  harmful  and 
&  sign  for  immediately  stopping  the  use  of  the  drug. 

POTASSIUM    IODIDE. 

Potassium  iodide  is  the  drug  which  is  most  widely  used  in  the  treat- 
ment of  all  forms  of  arteriosclerosis,  and  the  clinical  results  are 
so  definite  as  to  render  its  usefulness  certain.  The  manner  in  which  it 
€xerts  this  beneficial  action  is,  however,  much  less  definitely  known.  It 
was  at  first  supposed  by  Potain  and  others  to  lower  the  blood-pressure  by 
some  direct  action  upon  the  vasomotor  or  cardiac  mechanisms,  but  this 
action  is  slight  if  any,  and  the  writer  does  not  recall  ever  having  seen  high 
blood-pressure  depressed  by  potassium  iodide  without  the  intervention  of 
some  other  factor.  It  was  then  supposed  to  have  some  effect  in  diminish- 
ing the  viscosity  of  the  blood,  as  was  claimed  by  Otfried  Miiller  and  Inada 
in  Romberg's  clinic.  A  careful  persual  of  their  statistics  shows  that  the 
results  were  absolutely  negative  in  about  half  of  their  cases  and  within  the 
limits  of  observational  error  in  the  others.  Determann,  who  repeated  their 
■experiments,  found  the  effect  upon  viscosity  entirely  negative. 

It  was  then  claimed  by  Koranyi  and  others  that  potassium  iodide  pre- 
vented the  production  of  adrenalin  arterionecrosis,  but  this  claim  also  fell 
to  the  ground  when  tested  upon  a  very  large  series  of  animals  by  Leo  Loeb 
and  Githens. 

The  pharmacological  action  of  potassium  iodide  is  therefore  still  to 
be  classed  among  those  mysterious  actions  termed  "alterative." 

Some  light  is  thrown  upon  the  action  of  potassium  iodide  by  the  recent  studies  of 
Collins  and  Sachs  and  Longcope  upon  the  vascular  changes  due  to  syphilis.  These  ob- 
servers obtained  a  positive  Wassermann  reaction  in  many  cases  of  aortic  insufficiency 
in  which  there  was  no  other  sign  of  active  luetic  lesion.  In  these  cases  and  also  in  simple 
arteriosclerosis  of  luetic  origin,  the  potassium  iodide  probably  facilitates  the  removal  of 
the  luetic  exudations  and  thus  diminishes  the  ill  effects  of  the  arterial  lesion.  This  would 
explain  why  no  action  can  be  detected  upon  the  healthy  vessel  or  upon  the  mechanical 
factors  in  the  circulation. 

It  must  be  admitted  that  the  mode  of  action  is  entirely  unknown ;  but,  on 
the  other  hand,  administration  of  potassium  iodide  does  lessen  the  symp- 
toms of  stenocardia  and  other  painful  and  disagreeable  symptoms  in  many 
cases  of  arteriosclerosis,  and  may  even  cause  them  to  disappear  permanently. 
It  may  therefore  be  administered  with  advantage  in  all  cases  in  which  the 
above-mentioned  symptoms  arise  or  even  where  they  are  threatened. 

Potassium  iodide  is  best  given  after  meals  in  large  amounts  (half 
glassful  or  glassful)  of  water  or  milk.  The  unpleasant  taste  may  be  dis- 
guised by  a  little  sherry,  elixir  of  calisaya,  or  gentian.  Dose  potass,  iodi 
0.3  to  2.0  Gm.  (gr.  v  to  xxx)  (reached  by  increasing  doses). 


190  DISEASES   OF   THE   HEART   AND    AORTA. 

When  not  well  borne  by  the  stomach  or  when  the  heart  is  very  weak, 
sodium  iodide,  the  iodized  fatty  acid  "iodipin,"  or  new  iodized  organic 
acid  "sajodin"  may  be  substituted.  Their  action  does  not  seem  to  differ 
much  from  that  of  potassium  iodide. 

POTASSIUM  THIOCYANATE. 

Another  drug  which  tends  to  lower  the  blood-pressure  greatly  is  potassium  thiocya- 
nate  (KCNS).  The  use  of  this  drug  as  a  sedative  to  the  nervpus  system  was  first  suggested 
by  W.  Pauli  (1903),  who  believed  that  he  obtained  some  excellent  results  in  eleven  arterio- 
sclerotics and  in  two  cases  of  heart  failure.  It  was  used  more  carefully  by  J.  Pal  (1905), 
who  writes:  "I  have  been  able  to  obtain  a  good  effect  from  thiocyanate  preparations  in 
some  cases  in  which  even  potassium  iodide  was  without  effect.  This  cyanate  often  grad- 
ually reduces  a  high  blood-pressure,  but  often  brings  on  symptoms  of  intox- 
ication in  arteriosclerotics,  especially  in  those  with  renal  complications.  These  toxic 
symptoms  are  erythemata  and  mental  confusion,  which  disappear,  as  I 
have  found,  when  the  thiocyanate  is  left  off  and  opium  given.  .  .  .  Diuretin  and  iodide  or 
thiocyanate  are  of  value  (in  vasomotor  crises)  only  when  administered  over  long  periods." 

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VI. 

GYMNASTICS  AND  HYDROTHERAPY. 
GYMNASTICS. 

FUNDAMENTAL    PRINCIPLES. 

During  recent  years  gymnastic  exercises  have  come  to  play  a  major 
role  in  the  treatment  of  cardiac  diseases.  Although  this  treatment  was 
introduced  empirically,  its  physiological  basis  is  found  in  the  fact,  shown 
by  Frank  and  Hirschfelder,  that  a  strain  upon  the  ventricles  which  does 
not  exhaust  them  tends  to  act  as  a  stimulus  which  gives  rise  to  more  forci- 
ble contractions,  increases  their  tonicity,  and  causes  the  residual  blood 
(and  hence  the  dilatation)  to  decrease.  The  guiding  principle  is  further 
given  by  the  experimental  evidence  produced  by  these  writers,  that  when 
the  strain  was  excessive  it  had  the  opposite  effect,  and  caused  weakening 
of  the  contractions,  diminished  tonicity,  and  dilatation  of  the  heart.  (See 
Fig.  119,  page  136.) 

In  dealing  with  normal  individuals  it  is  observed  that  the  strengthen- 
ing of  every  normal  individual,  the  training  of  every  athlete  or  laborer  con- 
sists in  the  habituation  of  the  body,  and  particularly  of  the  heart,  to  gradu- 
ally increasing  muscular  effort  and  exercises.  (See  page  198.)  To  a  great 
extent,  as  has  been  seen,  page  129,  this  consists  in  securing  a  greater  increase 
in  output  of  blood  at  each  beat  without  calling  upon  any  of  the  accessory 
nervous  mechanism  to  bring  this  about.  Such  exercises  have  also  been 
used  with  great  success  in  the  treatment  of  patients  with  heart  failure.  It 
stands  to  reason  that  they  should  not  be  used  at  once  when  the  patient  is 
brought  in  with  an  acute  heart  failure;  but  after  a  sufficiently  long  period 
of  rest,  when  the  acute  condition  has  passed  off  and  he  can  sit  up  in  bed 
without  discomfort,  a  few  of  the  mildest  arm  movements  may  be  begun 
with  great  advantage.  It  is  often  better  to  train  the  patient  by  a  few  mild 
passive  or  resisted  movements  while  he  is  still  in  bed  than  to  subject 
him  at  once  to  the  strain  of  getting  up  for  an  hour  or  so  after  his  sojourn 
in  bed.  Moreover,  many  other  muscles  may  be  kept  in  tone,  the  blood- 
vessels in  the  muscles  may  be  kept  dilated,  and  the  resistance  to  blood 
flow  may  thus  be  diminished. 

SYSTEMS    OF    EXERCISE. 

In  accordance  with  these  facts  several  systems  of  exercises  have  been 
developed  for  assisting  in  the  training  of  the  heart.  In  all  of  them  the  cru- 
cial point  lies  in  the  avoidance  of  the  slightest  fatigue,  holding  of  the  breath, 
or  increased  breathing.  Hence  the  actual  result  obtained  depends  more 
upon  the  vigilance  and  intelligence  of  the  physician,  nurse,  or  attendant 
who  supervises  the  exercises  than  upon  the  exercises  themselves. 

13  193 


194  DISEASES   OF  THE   HEART    AND    AORTA. 

In  general  the  exercises  may  be  divided  into  four  classes: 

(1)  Passive  movements. 

(2)  Contraction  of  antagonistic  muscles. 

(3)  Resisted  movements. 

(4)  Mechanical  gymnastics. 

Passive  Movements. — These  are  the  mildest  possible  forms  of  exercise. 
The  attendant  grasps  the  patient  by  the  hands  or  feet  and  moves  these 
members  gently  and  slowly  about,  while  the  patient  makes  no  effort  at 
contraction  whatever.  Such  movements  have  the  effect  of  increasing 
the  circulation  of  lymph,  the  absorption  of  oedema,  and,  to  a 
certain  extent  also,  of  increasing  the  rapidity  of  blood  flow.  It  is  impor- 
tant to  avoid  all  exercises  in  which  the  arms  are  raised  high  above  the 
head,  since  this  hydrostatically  increases  the  pressure  in  the  vena  cava  and 
may  cause  momentary  dilatation  of  the  heart. 

The  following  exercises  or  modifications  of  them  may  be  carried  out 
while  the  patient  is  still  in  bed,  provided  the  greatest  precaution  is  used 
in  their  execution. 

(1)  Arms  horizontal,  to  the  front  and  back  to  the  Hne  of  the  shoulders. 

(2)  Arms  horizontal  in  line  of  shoulders,  thence  down  to  the  sides  of  the  body. 

(3)  Arms  horizontal,  describe  circles  with  hands. 

(4)  Arms  vertically  dependent  at  sides,  flex  and  extend  elbows. 

(5)  Arms  dependent  at  sides,  pronate  and  supinate  alternately. 

(6)  Clinch  and  open  fists. 

(7)  Legs  straight,  abduct;  then  adduct  thighs. 

(8)  Flex  and  extend  knee  at  side  of  couch,  never  raising  knee  above  level  of  body. 

(9)  Flex  and  extend  foot  at  ankle-joint. 

(10)  Rotate  thighs  internally  and  externally. 

(11)  Execute  small  circles  with  feet  without  raising  them  more  than  one  foot;    legs 

straight. 

Contraction  of  Antagonistic  Muscles. — Substantially  the  same  exercises 
may  be  carried  out  by  allowing  the  patient  himself  slowly  and  simultane- 
ously to  contract  both  the  muscles  concerned  in  the  movement  and  those 
which  antagonize  them, — i.e.,  biceps  and  triceps,  flexors  and  extensors  of 
wrist,  etc.  In  this  way  little  movement  is  made,  the  pulse-rate  is  slowed 
rather  than  accelerated,  and  yet  a  good  deal  of  energy  may  be  expended. 
The  blood-pressure  is  raised,  however.  If  the  patient  can  be  trained  to 
avoid  all  difficulty  in  breathing  and  all  discomfort,  a  good  deal  of  improve- 
ment in  muscular  strength  and  in  cardiac  tonicity  may  be  obtained  by 
this  method.  Its  main  drawback  lies  in  the  fact  that  the  intensity  of  the 
exercise  is  controlled  not  by  the  attendant  but  by  the  patient,  and  that 
the  latter  is  most  likely  to  do  more  than  is  beneficial. 

RESISTED    MOVEMENTS.       (SCHOTT   MOVEMENTS.) 

Probably  the  most  widely  used  of  all  the  cardiac  gymnastics  are  the 
passive  movements  introduced  by  August  Schott  of  Nauheim.  These  are 
generally  used  in  connection  with  the  Nauheim  baths.  This  combination 
is  particularly  advantageous  and  permits  at  once  of  all  the  advantages 
of  mild  exercise,  of  baths,  of  rest  and  stimulation  to  sleep,  of  psychic 
sedative,  and  of  the  psychic  suggestion  to  the  patient  that  a  great  deal  is 
being  done  and  a  great  effort  is  being  made  for  his  welfare. 


GYMNASTICS  AND   HYDROTHERAPY.  195 

The  Schott  movements  consist  of  practically  the  exercises  described 
above  carried  out  by  the  patient  himself,  but  with  an  attendant  who  makes 
a  slight  resistance  to  each  movement.  The  resistance  should  be  just  enough 
to  prevent  the  movement  from  being  made  rapidly,  and  at  no  time  should 
it  cause  the  patient  any  apparent  effort  or  increase  his  respirations.  Each 
day  the  resistance  may  be  increased  slightly,  so  that  in  a  short  time  the 
patient  may  be  doing  a  good  deal  of  work  without  realizing  it.  In  exe- 
cuting the  resistance  the  attendant's  mind  is  kept  fixed  upon  the  condition 
of  the  patient,  and  he  is  consequently  more  likely  to  notice  over-exertion 
in  the  latter  than  if  he  were  merely  supposed  to  watch  him  without  doing 
anything  himself.  In  carrying  out  the  Schott  movements  the  following 
rules  are  prescribed.^ 

Precautions  for  Schott  Exercises. — (1)  Each  movement  is  to  be  performed  slowly 
and  at  uniform  rate. 

(2)  No  movement  is  to  be  repeated  twice  in  succession  in  the  same  hmb  or  group 
of  muscles. 

(3)  Each  single  or  combined  movement  is  to  be  followed  by  an  interval  of  rest. 

(4)  The  movements  are  not  to  be  allowed  to  accelerate  the 
patient's  breathing,  and  the  operator  must  watch  the  face  for  the  slightest 
indications  of  (a)  dilatation  of  the  nostrils,  (b)  drawing  of  the  corners  of  the  mouth,  (c) 
duskiness  or  pallor  of  the  cheeks  or  lips,  (d)  yawning,  (e)  sweating,    (/)  palpitation. 

(5)  The  appearance  of  any  one  of  the  above  signs  of  distress  should  be  the  signal 
for  immediately  interrupting  the  movement  in  process  of  execution,  and  for  either  sup- 
porting the  limb  which  is  being  moved  or  allowing  it  to  subside  into  a  state  of  rest. 

(6)  The  patient  must  be  directed  to  breathe  regularly  and 
uninterruptedly,  and,  should  he  find  any  difficulty  in  doing  so,  or  for  any  reason 
show  a  tendency  to  hold  his  breath,  he  must  be  instructed  to  continue,  counting  in  a 
whisper  throughout  the  progress  of  each  movement. 

(7)  No  limb  or  portion  of  the  body  of  the  patient  is  to  be  so  constricted  as  to  compress 
the  vessels  and  check  the  flow  of  blood. 

Schott  Exercises. — The  following  is  a  list  of  Schott  exercises  in  the 
order  in  which  they  are  given.  The  resistance  is  moderate  and  steady,  the 
operator's  hand  always  being  applied  upon  the  surface  of  the  extremity 
toward  which  the  movement  is  made,  even  if  that  entails  gliding  around 
it  gently  during  the  movement.  Usually  the  operator's  hand  is  at  one  side 
of  the  patient's  limb  at  one  phase  of  the  exercise  and  at  the  opposite  when 
the  movement  is  reversed. 

1.  Arms  extended  in  front,  palms  facing  each  other.  The  operator's  palms  rest  upon 
the  backs  of  the  patient's  hands.  Patient's  arms  carried  backward  to  line  of  shoulders, 
the  movement  being  gently  resisted  by  operator  (Fig.  134).  The  operator's  palms  are  then 
rested  against  those  of  the  patient,  and  the  return  of  the  arms  in  front  of  the  chest  is  re- 
sisted. 

2.  One  arm  at  side,  elbow-joint  flexed  upward  to  shoulder,  then  extended  to  original 
position. 

3.  Arms  at  side,  raised  outward  till  thumbs  meet  over  the  head,  then  brought  back 
to  the  original  position. 

4.  Hands  at  level  of  pelvis  in  midline,  fingers  slightly  flexed.  Arms  raised  to  the 
vertex  of  the  head,  then  back. 

5.  Arms  at  sides,  then  raised  forward  in  parallel  planes  until  they  are  vertical,  then 
moved  back.  The  hand  of  the  operator  must  glide  around  the  wrist  so  that  it  is  always 
applied  to  antagonize  the  movement. 

^  Quoted  from  W.  Bezly  Thome. 


196 


DISEASES   OF  THE   HEART   AND    AORTA. 


6.  Trunk  flexed  on  hips,  knees  straight;   trunk  then  extended. 

7.  Trunk  rotated  without  movement  of  the  feet.    Operator  exerts  resistance  against 
the  shoulders. 


Fig.  134.- 
cated 


—Schott  resisted  movements.  (Modified  from  W.  Bezly  Thome.)  The  attendant's  hands  are  indi- 
in  black;  the  direction  of  the  movement  made  by  the  patient  is  indicated  by  the  black  arrows. 


8.  Tnmk  flexed  laterally,  first  to  one  side  then  to  the  other,  the  movement  being  an- 
tagonizisd  by  resistance  applied  in  the  axilla,  the  operator's  other  hand  resting  on  the  hip. 

9.  Movement  like  No.  2;  fists  clinched. 

10.  Same,  but  palmar  surface  of  fist  turned  outward. 

11.  Arm  extended  from  side,  palm  down,  raised  forwards  and  upwards  describing 
a  semicircle  imtil  it  is  raised  vertically  along  side  of  the  ear.    The  movement  is  then  reversed. 


GYMNASTICS  AND  HYDROTHERAPY. 


197 


12.  Arms  at  sides,  palms  inward,  moved  upwards  and  backwards  in  parallel  planes. 

13.  Patient  rests  one  hand  on  chair  or  table,  raises  knee  to  horizontal,  flexing  at  hip 
and  knee. 

14.  With  one  hand  resting  on  table,  patient  swings  extended  leg  forward  and  back- 
ward from  the  hip-joint. 

15.  Resting  with  both  hands  on  chair  in  front,  raises  foot  by  flexing  knee  without 
movement  at  hip. 

16.  Resting  one  hand  on  chair  at  side,  patient  swings  opposite  extended  leg  out- 
ward from  hip-joint,  then  returns  to  normal. 

17.  Arms  rotated  outwards  and  inwards  from  shoulder-joint,  operator  grasping  the 
metacarpal  portion  of  the  hand. 

18.  Wrist-joint  flexed  and  extended. 

19.  Ankles  dorsoflexed  and  extended  alternately. 

When  these  precautions  are  taken  the  exercises  have  an  excellent 
effect  in  a  considerable  number  of  cases,  bringing  about  relief  of  the  dilata- 
tion and  more  or  less  immediate  improvement  (increased  tonicity).  An 
example  of  this  is  shown  in  Fig.  135,  illustrating  the  diminution  in  the 
cardiac  shadow  under  the  X-ray  after 
a  very  few  resisted  movements.  On 
the  other  hand,  there  is  the  greatest 
danger  that  the  treatment  will  be  ap- 
plied in  cases  where  it  could  not  have 
been  expected  to  do  good  and  where 
it  actually  does  harm,  producing  over- 
strain and  decreased  tonicity  of  the 
cardiac  muscle. 

MECHANOGYMNASTICS. 

Movements  may  also  be  carried 
out  by  means  of  the  elaborate  and 
ingenious  apparatus  devised  by  Z  an  - 
d  e  r  for  regulating  them  in  direction 
and  intensity.  In  these  exercises  the 
movements  are  semi-passive,  being 
determined  to  a  great  extent  and  car- 
ried on  by  the  apparatus.  Hence  it 
becomes    more    difficult    to    control 

them  accurately  than  is  the  case  with  the  resistance  movements.  It  is 
unquestionable  that  excellent  results  have  been  obtained  by  this  method, 
especially  in  cases  where  there  is  mild  dilatation  but  no  serious  heart 
lesion;  but  it  is  certain  that  the  limits  of  the  patient's  strength  are  too 
readily  overstepped;  and  equally  certain  that,  in  the  large  institutions 
where  this  is  carried  out',  the  superintendents  usually  pay  so  little  atten- 
tion to  the  individual  patient  that  these  exercises  very  frequently  do  dis- 
tinct harm. 


Fig.  135.  —  Orthodiagraphic  outline  of  a 
patient  with  dilated  heart,  showing  the  effect  of 
Schott  movements.  (After  W.  Bezly  Thome.) 
Solid  line,  outline  before  treatment;  broken  line, 
outline  after  resisted  movements. 


WALKING    AND    CLIMBING. 


The  question  of  walking  involves  not  only  an  important  form  of  exer- 
cise treatment  but  also  the  regulation  of  the  convalescent's  daily  life.  As 
has  been  stated  above,  walking  up  and  down  stairs  frequently  introduces 


198  DISEASES   OF   THE   HEART    AND    AORTA. 

the  greatest  strain  upon  the  patient's  heart.  It  is  most  important  that  this 
strain  should  be  minimized.  This  may  be  done  by  causing  him  to  rest  upon 
each  step  long  enough  to  count  five,  ten,  or  twenty,  thus  insuring  him  against 
hurry  and  breathlessness  (J.  O.  Hirschfelder) .  Another  method  which  hai 
been  found  useful  was  suggested  by  the  writer's  wife  while  climbing  moun- 
tains in  the  Sierra  Nevadas.  She  noticed  that  she  could  climb  quite  steadily 
up  the  steepest  trails  provided  she  took  a  deep  or  normal  inspiration  each 
time  the  same  foot  touched  the  ground.  In  this  way  a  relation  was  estab- 
lished between  speed  and  respiration,  the  former  was  regulated  by  the 
latter,  and  a  certain  balance  maintained  between  the  rate  at  which  oxygen 
was  used  up  and  that  at  which  it  was  supplied.  As  the  pulse-rate  is  often 
some  definite  multiple  of  the  respiratory  rate,  this  procedure  also  tends  to 
regulate  the  former.  This  rhythm  is  one  which  is  very  satisfactory  for 
patients  with  heart  disease.  It  is  readily  acquired,  and,  having  once 
become  habitual,  does  much,  automatically,  to  keep  the  patient  within  his 
physiological  limits,  thus  enhancing  the  beneficial  effect  of  the  exercise 
while  establishing  a  safeguard  against  overstrain. 

Oerters  Mountain  Climbing. — Long  walks  and  mountain  climb- 
ing were  introduced  as  an  after-treatment  in  cardiac  disease  by  O  e  r  t  e  1 . 
Oertel  found  that  patients  convalescent  from  heart  failure,  and  especially 
those  suffering  from  fatty  infiltration  of  the  heart,  were  much  benefited 
by  long  walks  taken  slowly,  interrupted  by  frequent  rests.  Walks  along 
gradually  sloping  paths  in  the  mountains  were  most  beneficial,  and  in  fact 
became  a  feature  of  the  method.  This  is  designed,  however,  only  to  put 
the  finishing  touches  upon  the  treatment,  and  to  fit  the  patient  whose  heart 
is  already  in  good  working  order  for  the  more  strenuous  life  to  be  pursued 
after  his  discharge. 

CHOICE    OF    EXERCISE. 

As  regards  the  choice  and  use  of  exercise  in  treatment,  the  following 
general  principles  may  be  laid  down: 

(1)  No  exercise  should  be  begun  until  the  patient  has  been  under 
observation  for  a  few  days,  so  that  his  general  condition  is  thoroughly 
understood. 

(2)  If  the  patient  is  not  improving  under  absolute  rest,  exercises 
would  only  increase  the  work  imposed  upon  the  heart  and  would  do  harm. 

(3)  If  the  patient  has  improved  under  absolute  rest,  he  may  be  given 
one  or  two  passive  movements  (each  carried  out  five  or  ten  times)  two  or 
three  times  a  day,  and  the  exercises  very  carefully  increased  in  number 
and  intensity  each  day  before  allowing  him  to  get  out  of  bed.  Even  a  few 
mild  resisted  arm  exercises  may  be  tried,  bearing  in  mind  the  same  princi- 
ples, for  it  must  be  remembered  that  the  patient  may  obtain  much  more 
complete  and  immediate  rest  after  these  exercises  while  in  bed  than  when 
out  of  it,  and  also  that  he  is  not  at  the  same  time  subjected  to  the  strain 
of  standing.^ 

*  The  relative  mildness  of  such  exercises  in  patients  still  bed-ridden  is  seen  in  the 
fact  that  their  pulse-rate  and  respiration  return  at  once  to  normal  on  cessation  of  the  exer- 
cise. Physiologically,  to  exercise  in  the  horizontal  posture  increases  the  systolic  output 
more  and  changes  the  pulse-rate  less  than  in  the  erect  posture  (Erlanger  and  Hooker). 


GYMNASTICS  AND    HYDROTHERAPY.  199 

Once  out  of  bed  the  patient  should  at  first  be  given  a  day  or  two  of 
complete  rest  to  accommodate  himself  to  the  new  position.  Then  he  may 
be  allowed  to  begin  gradually  with  a  few  of  the  resisted  movements,  if  a 
competent  attendant  or  physician  can  supervise  them;  if  this  is  not  avail- 
able, he  may  be  allowed  to  practise  a  few  exercises  in  contracting  antago- 
nistic muscles  (Selbsthemmungsbewegungen) ,  at  first  under  the  direction 
of  the  physician,  later  under  the  observation  of  a  skilled  attendant,  or  of  some 
reliable  member  of  the  family  who  has  been  carefully  instructed  in  the  pre- 
cautions given  above.     About  this  stage  the  bath  treatment  may  be  begun. 

(4)  Mechanical  gymnastics  (with  the  Zander  apparatus  or  modifica- 
tions thereof)  can  be  recommended  only  when  supervised  by  persons  of 
great  experience  and  excellent  judgment. 

Training  at  End  of  Treatment. — (5)  When  the  patient  has  recovered 
somewhat,  but  not  sufficiently  to  withstand  the  wear  and  tear  of  daily 
life,  he  should  be  encouraged  to  take  short  walks,  gradually  lengthening 
the  space  covered,  at  first  about  the  hospital  grounds,  later  about  the 
city  or  country,  keeping  records 'of  the  distance  traversed  each  day.  He 
may  then  be  allowed  to  walk  up  hill.  Pari  passu  with  this  the  resisted 
or  antagonized  movements  and  the  baths  should  be  given.  Before  dis- 
charging the  patient,  he  should  be  compelled  to  take  some  regular  gym- 
nastic exercises  every  day  and  made  to  do  work  at  least  as  strenuous  as 
that  which  will  form  the  routine  of  his  daily  life  after  passing  from  under 
the  physician's  care.  It  is  no  more  fair  to  the  convalescent  to  put  him 
directly  back  from  the  sedentary  life  of  the  bedroom  or  the  hospital  to  the 
deadly  struggle  for  existence  outside  than  it  would  be  to  match  the  average 
citizen  against  a  prize-fighter.  He  must  be  gradually  trained  for  the  effort. 
This  principle  was  very  well  recognized  by  da  Costa  during  the  Civil  War. 
Before  sending  his  patients  back  to  their  regiments  where  they  were  subject 
to  heavy  field  duty,  forced  marches,  etc.,  he  kept  them  at  lighter  duties 
about  the  hospital,  upon  local  guard  duty,  etc.,  and  from  time  to  time 
during  this  period  subjected  them  to  tests  of  increasing  severity  (running 
races,  etc.)  until  he  was  quite  certain  of  their  ability  to  stand  the  strain. 
The  magnificent  results  which  he  reports  from  his  large  series  of  cases 
treated  under  otherwise  unfavorable  conditions  constitute  a  fitting  monu- 
ment to  one  of  America's  greatest  clinicians,  and  merit  the  careful  study 
of  all  who  would  learn  how  cures  should  be  obtained  in  heart  diseases. 

Treatment  and  Occupation. — On  the  other  hand,  the  training  to  which 
the  patient  need  be  subjected  should  be  suited  to  the  life  that  he  leads.  It 
would  be  unnecessary  to  train  a  clerk  in  a  store  up  to  the  point  of  muscyilar 
strength  that  is  necessary  for  the  ordinary  laborer.  But  it  is  necessary 
that  he  should  not  be  exhausted  by  a  few  hours'  standing  lest  the  cardiac 
overstrain  return.  On  the  other  hand,  when  restitutio  ad  integrum  has  not 
been  possible,  the  patient's  life  must  not  be  the  same  as  it  was  before  his 
illness.  His  work  must  be  cut  down.  This  may  often  be  done  in  the  more 
well-to-do  without  changing  the  business  by  employing  assistants  to  attend 
to  all  except  the  more  essential  affairs.  Poorer  persons  must  change  their 
occupations.  It  is  as  much  the  duty  of  the  physician  to  see 
that  this  is  done  after  the  recovery  as  it  was  his  duty 
during    the    height    of    the    illness    to    give    correct    treat- 


200  DISEASES   OF   THE   HEART    AND    AORTA. 

ment .  Otherwise  he  has  merely  prepared  the  patient  for  another  break- 
down. The  difficulty  in  finding  suitable  occupation  and  the  acumen  neces- 
sary in  meeting  changed  conditions  increase  rather  than  decrease  the 
responsibility  of  the  physician  in  this  regard.  He  must  see  to  it  that,  as 
stated  by  Professor  Osier,  "the  patient  must  always  live  within  his  income 
of  cardiac  energy."  His  mode  of  life,  and  especially  the  speed  of  his  move- 
ments and  the  intensity  of  his  efforts,  should  be  so  regulated  that  he  no 
longer  feels  at  any  time  palpitation,  shortness  of  breath,  or  precordial  pain. 

HYDROTHERAPY  IN  THE  TREATMENT  OF  HEART  DISEASES. 

Although  the  healing  power  of  mineral  springs  and  baths  was  thought 
by  the  older  physicians  to  be  well-nigh  universal,  the  scientific  application 
of  hydrotherapy  to  heart  disease  is  due  largely  to  the  studies  of  a  small 
group  of  men  at  Bad  Nauheim,  Germany.  Benecke,  in  1870,  noted  the 
favorable  action  of  baths  at  this  watering-place,  but  it  is  to  August  Schott 
that  is  due  the  real  credit  for  introducing  into  cardiac  therapy  what  is 
really  a  very  valuable  method  of  treatment. 

PHYSIOLOGICAL    ACTION    OF    BATHS. 

Physiologically  it  has  been  found,  especially  by  Erlanger  and  Plooker, 
and  a  little  later  by  Jacob  and  Strasburger,  that  all  baths  given  at  about 
the  temperature  at  which  the  body  neither  gives  off  nor  loses  heat  (92°  F., 
33°  C.)  increase  the  pulse-pressure  and  slow  the  pulse-rate.  Strasburger 
found  this  to  be  particularly  true  as  regards  baths  of  the  same  composition 
as  those  at  Nauheim,  or  indeed  any  other  baths  in  which  COj  is  effervescing; 
and  ascribes  this  action  to  the  dilatation  of  the  vessels  in  the  skin  over  the 
whole  body,  as  well  as  to  the  cardiac  reflexes  from  stimulation  of  the  sensory 
nerves  by  the  prickling  sensation  of  the  COj.  These  effects  in  themselves 
would  be  sufficient  upon  a  priori  grounds  to  indicate  a  probable  value  of 
such  baths  in  weakened  hearts.  Schott's  treatment  has,  however,  long 
antedated  these  explanations.  Schott,  Thorne,  Schminke,  and  a  host  of 
other  observers  have  demonstrated  that  the  area  of  cardiac  dulness  and 
the  X-ray  shadow  of  the  heart  diminished  after  such  a  bath  (cardiac  tonicity 
increased). 

An  excellent  treatise  of  his  results  and  those  obtained  by  other  ob- 
servers is  given  in  extenso  in  English  in  the  monograph  of  W.  Bezly  Thorne, 
to  which  the  reader  is  referred  for  details  of  the  method.  Other  excellent 
accounts  are  given  by  Satterthwaite,  P.  K.  Brown,  et  al. 

PRECAUTIONS. 

The  baths  should  not  be  given  to  patients  who  are  in  the  extreme 
stages  of  cardiac  break-down,  nor  indeed  to  any  very  weak  patients,  until 
they  have  been  prepared  for  the  slight  strain  which  accompanies  them  by 
some  course  of  mild  exercises,  preferably  resistance  exercises  (see  page  195). 
They  should  never  be  taken  less  than  one  or  two  hours  after  a  light  meal 
or  four  to  five  hours  after  a  heavy  one,  and,  on  the  other  hand,  should  not 
be  given  upon  an  absolutely  empty  stomach. 


GYMNASTICS  AND   HYDROTHERAPY.  201 


NATURAL    AND    ARTIFICIAL    NAUHEIM    BATHS. 

The  Naiiheim  baths  are  obtained  from  several  mineral  springs  of  different  com- 
position. A  course  of  baths  is  begun  in  the  Great  Sprudel  (composition  H2O  1000,  NaCl 
2.18,  KCl  0.5,  CaCU  1.7,  MgClj  0.4,  calcium  bicarbonate  2.3,  CO,  3.17;  temperature  31.6°  C, 
88.8°  F.),  most  of  the  COj  being  allowed  to  escape  before  immersion  of  the  patient. 

The  effect  of  the  Nauheim  baths  can  be  imitated  at  home  or  in  the  hospital  by  add- 
ing the  same  salts  to  the  water  in  the  bath-tub.  A  great  variety  of  such  artifi- 
cial Nauheim  salts  are  on  the  market,  put  up  in  packages  ready  for  use.  The 
most  satisfactory  known  to  the  writer'  contains: 

Grammes.     Pounds.     Per  cent. 

Sodium  chloride 3500  8  2.2 

Calcium  chloride  (magnesium  chloride) 900  2  0. 53 

Sodium  bicarbonate 800  If  0.1 

Sodium  bisulphate  yielding  CO^ 1000  2 J  0. 29 

In  order  to  prevent  the  bisulphate  from  injuring  the  tub  it  is  advisable  to  cover  the 
walls  and  floor  of  the  latter  with  a  large  sheet  of  rubber  cloth  about  6  x  8  ft.  in  size.  The 
bath  is  filled  with  warm  water,  90°-95°F.  (a  good-sized  bath  requires  40  to  45  gal. — 150  to 
175  litres)  and  the  salts  added — first  the  sodium  chloride,  then  the  calcium  chloride,  then 
the  sodium  bicarbonate,  and  lastly  the  acid  sulphate  (NaHC03  +  NaHS04  =  Na2SOi+C02  + 
H2O).     The  effervescence  continues  throughout  the  bath. 

CAUTIONS    IN    GIVING    BATHS. 

In  preparing  the  first  bath  it  is  better  to  begin  with  half 
strength  of  the  salts  or  even  less.  The  patient  is  allowed  to  remain  in 
this  bath  not  longer  than  fifteen  minutes,  being  watched  care- 
fully during  this  time  and  removed  at  once  if  there  is  the  slightest 
increase  in  cyanosis  or  real  discomfort  of  any  kind — flushing, 
excitement,  or  syncope.  "The  immediate  effect  of  the  first  few  baths  is  to 
produce  a  sense  of  oppression  at  the  precordium,  under  the  influence  of 
which  the  patient  breathes  slowly  and  deeply  for  two  or  three  minutes. 
Respiration  then  becomes  easy  and  continues  slower  by  from  two  to  four 
breaths  a  minute,"  after  which  the  symptoms  subside.  In  general  the  effect 
should  be  similar  to  thut  in  the  following  case  quoted  from  Thorne: 

"A  patient,  aged  46,  whose  health  had  been  declining  for  years,  was  found  to  have 
a  pulse  of  80  in  the  recumbent,  and  of  88  in  the  sitting,  position.  While  he  stood  it  varied 
from  100  to  104,  and  if  he  walked  ten  paces  it  rose  from  120  to  130.  The  apex  was  found 
to  beat  an  inch  outside  the  nipple  line.  Within  two  minutes  of  immersion  in  his  first 
thermal  bath  the  pulse  had  fallen  to  70,  and  judged  by  the  finger  appeared  to  have  doubled 
its  volume;^  at  the  end  of  four  minutes  it  was  68,  in  six  minutes  66,  in  eight  minutes  68, 
and  while  standing  after  the  bath  it  was  90.  Before  he  left  the  bath  after  an  immersion 
of  ten  minutes,  the  apex  beat  was  found  to  have  receded  half  an  inch  in  the  direction  of 
the  mesial  line,  and  nails  and  fingers,  which  had  been  snow-white  up  to  the  junction  of 
the  second  with  the  first  phalanx,  had  assumed  a  healthy  flesh  tint. " 

This  healthy  reaction  of  the  skin  should  be  present  within  a  few  minutes 
after  the  bath.     Its  absence  indicates  that  the  treatment  has  been  too 

'  Put  up  by  R.  R.  Rogers  Chemical  Co.,  San  Francisco.  This  preparation  is  partic- 
ularly useful,  owing  to  the  excellent  grade  of  sodium  bisulphate  prepared  and  the  perma- 
nent and  convenient  form  in  which  it  is  put  up.  Moreover,  the  sodium  bisulphate  is  put  up 
in  lumps  the  size  of  a  hazel-nut,  which  allows  the  CO2  to  be  generated  uniformly  through- 
out the  bath. 

^  Probably  the  pulse-pressure  had  actually  doubled. 


202  DISEASES   OF  THE   HEART   AND    AORTA. 

violent,  too  prolonged,  or  in  other  ways  unsatisfactory,  and  unless  this  can 
be  obviated  after  the  next  bath  or  two  the  treatment  should  be  discontinued. 
After  the  bath  the  patient  should  be  made  to  lie  down  and  rest,  if 
possible  to  sleep,  for  at  least  an  hour  before  leaving  the  building  or  doing 
anything  else,  and  upon  this  rest  as  much  as  anything  else  depends  the 
success  of  the  treatment. 

BIBLIOGRAPHY. 

Gymx.\stics  axd  Hydrotherapy. 

Herz,  M.:  Lehrbuch  der  Heilgymnastik,  Berl.  and  Vienna,  1903. 

Schott,  Aug.:  Zur  Therapie  der  chronischen  Herzkrankheiten,  Berl.  klin.  Wchnschr.,  1885. 
Thome,  W.  B.:  The  Schott  Methods  in  the  Treatment  of  Chronic  Diseases  of  the  Heart. 
Nebel:  Bewegungskuren  mittelst  schwedischer  Heilgymnastik  und  Massage  mit  besonderer 

Beriicksichtigung  der  mechanischen  Behandlung  des  Dr.  CI.  Zander,  Wiesbaden,  1889. 
Oertel:  Ueber  Terrainkurorte,  Leipz.,  1886.     Ueber  die  chronischen  Herzmuskelerkrank- 

ungen  und  ihre  Behandlung,  Verhandl.  d.  Kong.  f.  inn.  Med.,  Wiesb.,  1888,  v,  13. 

Allgemeine  Therapie  der  Kreislaufstorungen,  1891,  4th  ed. 
Beneke,  F.  W,:  Ueber  Nauheim's  Soolthermen,  Marburg,  1859;    Weitere  Mittheilungen 

ueber  die  Wirkung  der  Soolthermen  Nauheims,  Marburg,  1861;    Nauheim's  Soolther- 
men gegen  Gelenkrheumatismus  mit  oder  ohne  Herzaffection.,  Berl.  klin.  Wchnschr., 

1870,  269. 
Schott,  A.:  Die  Wirkung  der  Bader  auf  das  Herz,  ibid.,  1880,  xvii,  357,  372. 
Erlanger  and  Hooker,  1.  c,  page  35. 
Strasburger,   J.:  Ueber   Blutdruck,  Gefasstonus  und   Herzarbeit   bei   Wasserbadern  ver- 

schieder  Temperatur  und  bei  Solbadern,  Deutsches  Arch.  f.  klin.  Med.,  Leipz.,  Ixxxii, 

459. 
Satterthwaite:  Nauheim  Methods  in  Chronic  Heart  Disease  with  American  Adaptations, 

Internat.  Clin.,  Phila.,  1903,  13  ser.,  i,  52. 
Brown,  P.  K.:  Artificial  Nauheim  Baths  in  Chronic  Heart  Cases,  Boston  M.  and  S.  J.,  1906, 

civ,  276. 


VII. 

HYPERTROPHY   AND    ATROPHY. 

HYPERTROPHY. 

To  enable  the  heart  to  recover  from  an  overstrain  and  the  consequent 
dilatation,  to  maintain  the  circulation  in  the  presence  of  a  valvular  lesion 
or  dilatation,  or  to  reestablish  compensation  once  broken,  it  must  put  forth 
an  increase  in  force.  The  stimulus  for  this  seems  to  lie  in  the  increase  in 
residual  blood  in  the  ventricle,  which  acts  as  an  increase  in  load  upon  the 
heart  muscle,  and  thus  tends  to  increase  both  irritability  and  force  of  con- 
traction, as  shown  by  O.  Frank  (see  page  135),  and  particularly  to  bring 


Fig.  136. — Hypertrophic,  normal,  and  atropine  hearts.     (From  .specimens  in  the  Army  Medical  Museum, 

Washington,  D.  C.) 

about  an  increase  in  tonicity.  It  seems  probable  that  this  increase  in 
tonicity  is  of  primary  importance  as  a  predisposing  factor  to  hypertrophy, 
and  Barcroft  and  Dixon  have  shown  that  increased  tonicity  is  accompanied 
by  an  increased  CO,  metabolism  in  the  heart. 


PATHOLOGICAL    ANATOMY. 

Changes  in  the  Fibres. — ^The  main  visible  change  which  the  heart  muscle  undergoes 
is  a  swelling  of  the  individual  fibres  (Tangl,  Goldenberg,  Dehio,  R.  M.  Pearce)  with  little 
if  any  multiplication  of  the  muscle-cells.  Goldenberg  finds  that  the  muscle-cells  in  the 
wall  of  the  hypertrophic  heart  have  a  diameter  of  17.65  fJ-,  in  the  normal  heart  12.85  /^, 
and  in  the  atrophic  heart  10.84  ;".  The  striation  of  the  fibres  also  becomes  less  distinct, 
and  vacuoles  appear  in  the  sarcoplasm,  changes  which  are  similar  to  what  is  observed  in 

203 


204 


DISEASES   OF   THE    HEART    AND    AORTA. 


a  striated  muscle  as  the  result  of  prolonged  contraction.  Ranke  has  shown  that  in  skeletal 
muscle  these  changes  are  due  to  imbibition  or  endosmosis  of  water,  which,  according  to 
the  beautiful  experiments  of  J.  Loeb  and  his  pupil,  Miss  Cooke,  is  brought  about  in  the 
following  way:  During  the  muscular  contraction  the  more  complex  molecules  break  down 
into  several  simpler  ones,  thereby  increasing  the  number  of  molecules  in  solution  in  the 
muscle  plasma,  the  osmotic  pressure  rises,  and  hence  brings  about  an  endosmosis  of  water 
into  the  fibres.  Having  once  entered,  the  water  molecules  remain  and  the  muscle  swells. 
There  can  be  Uttle  doubt  that  the  same  process  is  going  on  in  cardiac  muscle,  especially 
when  subjected  to  overwork,  but  no  observations  have  actually  been  made  upon  this 
phase  of  the  subject.' 

In  cardiac  hypertrophy  three  anatomical  changes  may  be  said  to  take 
place  simultaneously:  (1)  an  increase  in  size  of  the  individual  muscle- 
cells,  but  apparently  no  increase  in  their  number;  (2)  a  certain  amount  of 


Fig.  137. — Photomicrographs  of  atrophic  and  hypertr<.:  i-cle.      A.  Atrophic  heart 

muscle,  showing  small  cells.  The  specimen  also  shows  some  oedema  and  slight  mononuclear  infiltration 
between  the  muscle  cells.     B.  Hypertrophic  heart  muscle  showing  large  cells  with  swollen  nuclei. 

degeneration  is  almost  always  present  in  some  of  the  muscle-cells;  (3)  a 
proliferation  of  the  strands  of  connective  tissue  between  the  bundles  of 
muscle-fibres  (interfascicular  myofibrosis,  see  page  234). 

Dehio  and  Pearce  have  shown  that  each  fibre  may  pass  through  the 
following  stages:  normal  -*  hypertrophy  —  degeneration,  the  latter  stage 
being  associated  with  proHferation  of  interstitial  connective  tissue  (myo- 
fibrosis). Accordingly,  we  may  find  the  heart-cells  in  the  following  con- 
ditions: 

(1)  Normal +  hypertrophied  (heart  somewhat  enlarged:  as  in  athletes,  also  in  Kiilbs's 
dogs). 

(2)  Hypertrophied  +  degenerated;  some  proliferation  of  connective  tissue  (heart 
much  enlarged — cor  bovinum;  still  strong). 

(3)  Degenerated.  Marked  proliferation  of  connective  tissue.  Marked  weakness  of 
the  heart.    Large  failing  heart.     Hypertrophy  +  dilatation  (digitalis  often  harmful). 


*  Fleischer  and  Leo  Loeb  have  advanced  the  same  explanation. 


HYPERTROPHY  AND  ATROPHY.        '  205 

Types  of  Hypertrophy. — Hypertrophy  was  supposed  by  Cohnheim  to 
assume  three  types: 

(1)  General  concentric  hypertrophy,  involving  all  the 
chambers  of  the  heart  about  equally. 

(2)  Local  concentric  hypertrophy,  involving  the  walls 
of  one  or  more  chambers  of  the  heart  which  is  subjected  to  extra  work. 
The  fibres  are  not  especially  elongated, 

(3)  Local  (excentric)  hypertrophy  with  elongation  of 
the  muscle-fibres,  as  in  aortic  insufficiency.  The  elongation  of  the  fibres  is 
somewhat  out  of  proportion  to  the  increase  in  size  of  the  heart. 

The  existence  of  these  three  types  of  hypertrophy  as  separate  entities 
was  already  disputed  by  Cruveilhier  in  1833.  It  is  probable  that  the  size 
of  the  cavities  as  found  at  autopsy  bears  no  constant  relation  to  that  pres- 
ent during  life.  Moreover,  the  ventricular  cavities  in  cases  of  chronic 
nephritis  are  often  quite  as  large  as  those  in  hearts  of  aortic  insufficiency, 
though  the  former  typifies  the  so-called  concentric,  the  latter  the  excentric 
hypertrophy. 

Occurrence  and  Sites  of  Hypertrophy. — The  relative  frequency  with 
which  these  factors  occur  in  cases  of  hypertrophy  is  shown  in  the  following 
statistics  compiled  by  W.  T.  Howard  from  autopsies  made  in  the  Patho- 
logical Department  of  the  Johns  Hopkins  Medical  School  upon  108  subjects 
showing  hypertrophy  of  the  heart. 

Cases.  Per  cent. 

Arteriosclerosis 65  59 

Nephritis 14  13.4 

Valvular  lesions  of  the  heart 13  12.4 

Adherent  pericardium 8  7.6 

Hard  work 4  3.8 

Tumors 2  1.9 

Aneurism  of  the  heart  wall 1  0.95 

Hsemic  plethora 1  0 .  95 

Total 108  100 

The  right  ventricle  showed  hypertrophy  in  70  cases  (66  per  cent.),  of 
which  there  were — 

Arteriosclerosis  (often  of  pulmonary  artery),  52;  adhesive  pericarditis,  6;  valvular 
lesions,  8;  chronic  nephritis,  3;  hydraemic  plethora,  1. 

Hypertrophy  of  the  auricles  (atria)  was  most  marked  in  mitral  stenosis 
and  adhesive  pericarditis. 

Strain,  Exercise,  and  Hypertrophy. — In  normal  individuals  the  weight 
of  the  heart  is  almost  proportional  to  the  weight,  not  of  the  entire  body, 
but  of  the  musculature  (W.  Miiller,  Hirsch),  being  relatively  low  in  fatty 
and  relatively  high  in  muscular  individuals.  The  absolute  weight  of  the 
heart  is  about  jj-^  (.0059)  of  the  body  weight  in  men,  yj-^  (.00546)  in 
women.  The  same  general  principle  applies  in  animals,  the  most  active 
animals  having  the  largest  hearts,  especially  race-horses,  hares,  etc.,  as 
compared  to  less  active  members  of  the  same  species. 

When,  however,  the  heart  is  subjected  to  abnormal  strain,  especially 
as  the  result  of  valvular  lesion,  it  hypertrophies  and  increases  in  size  to 
dimensions  which  are  often  enormous.     It  is  not  very  uncommon  to  find 


206  DISEASES   OF  THE   HEART    AND    AORTA. 

hearts  of  twice  or  even  three  times  the  normal  size  (500  to  800  Gm.,  17  to 
26  oz.),  and  in  the  Army  Medical  Museum  in  Washington  there  is  a  speci- 
men of  one  weighing  1000  Gm.  (33  oz.).  Another  heart  of  1400  Gm.  (46i 
oz.)  has  been  reported.  Such  a  heart  is  usually  designated  as  a  beefy 
heart  or  cor  bovinum,  indicating  the  animal  to  which  its  size  would  be 
proportioned. 

Work  Hypertrophy. — Whether  a  true  hypertrophy  occurs  in  a  per- 
fectly healthy  heart  has  been  much  disputed,  many  writers  taking  the 
stand  with  Romberg  that,  ''though  the  possibility  of  a  'work  hypertrophy' 
cannot  be  denied,  more  proofs  of  its  existence  are  necessary." 


Fio.  138. — Heart  (A)  of  normal  dog  and   (B)  of  dog  which  has  run  for  three  months  on  a  tread-mill. 
(After  Kulbs,  Arch.  j.  exper.  Path.  u.  Pharmacol.,  Iv.) 

Recently,  however,  absolute  proof  of  a  work  hypertrophy  without  myocardial  degen- 
eration has  been  brought  by  the  beautiful  experiments  of  Kulbs.  This  observer  took  two 
dogs  of  the  same  litter  and  of  equal  size,  kept  them  in  neighboring  cages  upon  the  same 
diet,  but  compelled  one  of  them  to  run  upon  a  tread-mill  daily  for  three  to  six  months, 
while  the  other  was  kept  quiet  and  used  as  a  control.  At  the  end  of  this  time  both  dogs 
were  killed  in  the  same  manner. 

First  set.  Second  set. 

Work  do?.        Control.        Work  dog.       Control. 

Total  weight 15,200         15,000         19,200         20,400 

Musculature 5,696  5,342  6,489  6,776 

Heart 152  99  172  113 

Kulbs's  results  have  been  confirmed  by  Grober  and  by  Joseph. 

The  increase  in  size  of  the  heart  was  not  accompanied  by  any  change  in  the  skeletal 
musculature,  nor  were  any  pathological  changes  present  in  the  heart  or  arteries.  The 
muscle  here  simply  underwent  an  increase  in  size,  the  purest  form  of  hypertrophy.  Kulbs's 
dogs  were  simply  in  training  to  run  on  a  tread-mill.  The  process  was  exactly  the  same  as 
the  "training"  of  an  athlete,  and,  clinically,  it  is  often  found  that  athletes  have  mildly 
hypertrophied  hearts.  Schieffer  has  demonstrated  with  the  orthodiagraph  that  the  size 
of  the  heart  is  increased  in  persons  whose  occupations  require  hard  work  and  decreased  in 
those  with  sedentary  callings.  He  has  also  shown  that  the  hearts  of  the  young  men  doing 
military  service  in  the  German  Army  increase  in  size  somewhat  during  their  period  of 
service.  However,  these  men  often  indulge  in  excess  of  alcohol  or  tobacco,  so  that  before 
they  die  enough  myocardial  change  has  set  in  to  justify  the  scepticism  of  men  like  Krehl 
(I.e.)  and  Romberg  (I.e.).  Nevertheless,  though  a  true  "work  hypertrophy"  must  be 
admitted,  in  these  experiments  it  is  noticeable  that  the  yicrease  in  weight  of  the  heart 


HYPERTROPHY  AND  ATROPHY.  207 

amounted  to  only  52  per  cent,  as  compared  with  changes  of  100  to  300  per  cent,  often 
observed  in  man.  It  is  doubtful  whether  a  corresponding  degree  of  hypertrophy  would 
be  noticeable  clinically. 

ETIOLOGICAL    FACTORS. 

Hypertrophy  in  Chronic  Nephritis. — The  most  remarkable  and  most 
important  of  all  these  forms  of  hypertrophy  is  that  taking  place  in  chronic 
nephritis.  This  was  first  noticed  by  Richard  Bright  in  his  classical  descrip- 
tion of  dropsy  in  nephritis. 

In  18.53,  Wilkes  thought  that  the  lesions  of  the  kidneys  and  arteries  were  part  of  the 
same  morbid  condition;  while  Gull  and  Sutton  assumed  that  the  general  arteriocapillary 
fibrosis  brought  about  an  increased  resistance  through  narrowing  of  the  arterial  bed,  and, 
as  a  result  of  this,  high  blood-pressure  and  hypertrophy  of  the  heart.  Senator  ascribed  the 
hypertrophy  to  a  "  dyscrasic "  property  of  the  blood  in  nephritis,  stimulating  the  heart 
to  contractions  of  abnormal  force.  Passler  and  Heineke  have  recently  subjected  the 
matter  to  critical  experiment.  They  found  that  if  they  cut  out  pieces  of  kidney  from  a 
dog  bit  by  bit  until  renal  substance  equal  to  Ih  kidneys  had  been  removed,  the  heart  then 
began  to  hypertrophy  and  the  blood-pressure  to  rise.  If  considerably  more  tissue  was 
removed,  the  animal  became  cachectic,  the  blood-pressure  remained  low,  and  the  heart 
did  not  hypertrophy.  They  ascribed  these  cardiac  changes,  as  George  Johnson  had  done, 
to  the  presence  in  the  blood  of  some  substance  having  a  digitalis-like  action,  being  either 
retained  in  the  circulatipn  in  abnormally  large  quantities  as  the  result  of  disturbed  excre- 
tion, or  being  a  true  internal  secretion  from  the  diseased  kidney.^ 

Numerous  other  theories  of  cardiac  hypertrophy  in  renal  disease  have  been  advanced. 
Chief  among  these  is  the  theory  of  J.  Cohnheim  and  Traube  that  the  sclerosis  of  renal 
vessels  narrowed  the  arterial  bed  in  the  kidney,  thereby  introducing  an  increased  resistance 
into  the  general  circulation,  and  that  these  changes  in  the  renal  vessels  were  enough  to 
raise  the  general  blood-pressure.  It  would  appear  in  the  light  of  more  modern  research 
that  this  cutting  off  of  the  blood  stream  is  in  itself  insufficient.  On  the  other  hand.  Buhl, 
Huchard,  and  Albrecht  have  suggested  that  the  hypertrophy  is  not  a  true  one  but  simply 
a  pseudohypertrophy  (interfascicular  myofibrosis,  see  page  234),  the  entire  increase  in 
size  of  the  heart  being  due  to  growth  of  connective  tissue  and  not  of  the  heart  muscle,  but 
histological  examinations  do  not  bear  out  this  view. 

Hypertrophy  from  Overdrinking. — Closely  allied  to  this  condition  is  the 
tremendous  heart  hypertrophy  which  is  universally  found  to  result  from 
drinking  large  quantities  of  beer,  and,  since  it  does  not  accompany  excess 
in  any  other  form  of  alcohol  to  the  same  extent,  it  is  thought  to  be  due  to 
the  large  quantity  of  fluid  ingested.  That  increase  in  the  fluid  in  the  blood 
at  once  results,  not  so  much  in  a  rise  in  arterial  blood-pressure  as  in  rise  in 
venous  blood-pressure,  dilatation  of  the  heart,  and  increases  in  the  systolic 
output,  even  to  the  point  of  doubling  or  trebling  it,  can  easily  be  shown 
with  Henderson's  cardiometer,  and  this  no  doubt  illustrates  the  mechanism 
by  which  the  change  is  brought  about. 

Hypertrophy  and  Arteriosclerosis. — The  relation  of  hypertrophy  of  the 
heart  to  arteriosclerosis  independent  of  any  renal  changes  is  also  of  funda- 
mental importance.  The  coincidence  of  the  two  conditions  in  the  same 
individual  has  long  been  noted,  and  both  have  been  brought  about  experi- 
mentally by  administration  of  certain  poisons,  notably  adrenalin  (Josue, 
Erb,  Pearce,  et  al.). 

'  Tigerstedt  and  Bergmann  (Skand.  Arch.  f.  Physiol.,  Leipz.,  1898,  viii,  224)  found  that 
injection  of  renal  extract  actually  raised  the  blood-pressure,  owing  to  the  presence  of  a 
substance  which  they  named  "renin.'' 


208  DISEASES   OF   THE    HEART   AND   AORTA. 

Cardiac  and  Adrenal  Hypertrophy. — A  new  light  has  been  thrown  upon 
the  subject  by  the  studies  of  Vaquez  and  Aubertin  (1905),  Aubertin  and 
Clinet,  Wiesel,  p,nd  Gaillard. 

Aubertin  was  able  to  produce  cardiac  hypertrophy  in  rabbits  by  various  means, 
and  found  in  every  case  a  simultaneous  hyperplasia  of  the  medullary 
substance  in  the  adrenals.  A  similar  finding  had  been  made  by  Vaquez  and 
Aubertin  in  cases  of  chronic  nephritis  associated  with  hypertrophy  of  the  left  ventricle, 
which  was  confirmed  by  Wiesel  in  1907.  In  December,  1907,  Aubertin  and  Clunet  made 
a  study  of  120  unselected  autopsy  cases.  Of  these  18  showed  very  definite  hypertrophy 
of  the  medulla  of  the  adrenals,  and  16  of  these  18  showed  marked  hypertrophy  of  the 
heart.  On  the  other  hand,  but  10  of  these  hypertrophied  hearts  were  associated  with  renal 
disease:  the  others  occurred  in  conjunction  with  valvular  lesions,  congenital  defect  in  the 
septum  ventriculorum,  aortic  sclerosis,  etc.  Aubertin,  however,  states  very  definitely  that 
besides  these  groups  they  encountered  cases  of  cardiac  hypertrophy  without  the  existence 
of  adrenal  hyperplasia,  so  that  this  association  is  not  invariable;  and  they  conclude  that 
it  is  at  present  impossible  to  decide  whether  the  cardiac  hypertrophy  occurs  as  a  result  of 
oversecretion  of  adrenalin,  or  whether  the  hyperplasia  of  the  adrenals  occurs  as  a  result 
of  slight  venous  stasis  in  those  organs  while  the  hypertrophy  is  going  on.  Arteriosclerosis 
was  the  rule  but  not  invariably  in  these  cases  with  adrenal  hypertrophy. 

It  must  be  noted  that  the  action  of  adrenalin  is  just  that  which  might  be  expected 
to  bring  about  hypertrophy  of  the  heart,  for  it  causes,  (1)  a  general  vasoconstriction; 
(2)  a  marked  increase  in  the  tonicity  of  the  heart;  (3)  an  increase  in  the  force  of  the  beat 
and  in  the  systolic  output. 

However,  the  results  of  Cohn,  under  Aschoff's  direction,  are  less  favor- 
able to  this  theory.  In  12  cases  of  hypertrophy  of  the  left  ventricle  with 
chronic  nephritis,  he  found  hypertrophy  of  the  adrenal  cortex  in  only  3 
(25  per  cent.),  while  in  23  cases  of  chronic  nephritis  without  hypertrophy 
of  the  heart  he  found  hypertrophy  of  the  adrenal  cortex  in  8  (34  per  cent.). 
These  findings  tend  to  throw  considerable  doubt  upon  the  theory  of  Vaquez 
and  Wiesel. 

Hypertrophy  and  Abdominal  Arteriosclerosis. — Hasenfeld  has  found 
that  no  hypertrophy  sets  in  unless  arteriosclerosis  is 
present  in  the  aorta  above  the  level  of  the  superior 
mesenteric  artery.  Practically  all  the  substances  which  are  known 
to  bring  on  arteriosclerosis  are  vasoconstrictors,  and  beginning  arteriosclero- 
sis in  man  seems  usually  to  be  accompanied  by  vasoconstriction.  It  is 
readily  conceivable  that  any  sclerotic  obstruction  below  the  mesenteric 
would  be  easily  compensated  for  by  dilatation  of  the  abdominal  vessels, 
and,  consequently,  would  bring  about  no  increased  resistance  to  blood  flow, 
while  at  the  higher  level  the  presence  of  sclerosis  is  more  or  less,  equivalent 
to  clamping  the  abdominal  aorta. ^ 

DIAGNOSIS. 

It  would  appear  at  first  sight  to  be  extremely  easy  to  determine  clini- 
cally whether  in  a  given  case  hypertrophy  is  present  or  not,  and  the  older 
clinicians  laid  down  very  definite  rules  for  its  detection,  most  of  which  were 
fallacious.  In  general,  we  may  agree  with  Gibson  that  the  most  important 
signs  of  hypertrophy  of  the  left  ventricle  are  increase  in  cardiac  dulness  to 
the  left,  with  a  more  or  less  steady,  forceful,  and  "heaving"  impulse,  and  a 

'  An  excellent  discussion  of  the  theoretical  and  experimental  side  of  the  question  is 
given  by  R.  M.  Pearce. 


HYPERTROPHY  AND  ATROPHY. 


209 


booming  first  sound  of  low  pitch,  and  an  accentuated  second  sound  at  apex 
and  aortic  area.  These  signs  are  dependent  largely  upon  the  contact  of  the 
heart  with  the  chest  wall;  and  if,  as  is  often  the  case  in  an  emphysematous 
individual,  the  lung  intervenes  between  the  left  border  of  the  heart  and  the 
chest  wall,  all  the  signs  may  be  diminished  beyond  recognition.  The  diag- 
nosis may,  however,  often  be  made  from  the  history  in  spite  of  the  clinical 
findings.  Thus,  if  an  aortic  or 
mitral  insufficiency  has  persisted 
for  some  time  and  the  heart  is 
in  a  condition  of  moderate  vigor 
with  a  normal  pulse-rate,  it  may 
be  assumed  that  hypertrophy  of 
the  heart  has  had  to  take  place 
in  order  to  maintain  the  circula- 
tion, in  spite  of  distant  heart 
sounds  and  absence  of  the  apex 
beat.  Prolonged  high  blood- 
pressure  is  usually  associated 
with  some  degree  of  hypertrophy 
of  the  left  heart,  but  not  invari- 
ably. In  differentiating  from 
dilatation  it  may  be  stated  that, 
except  under  unusual  conditions 
brought  on  by  stimulation  of  the 
vagus,  the  factors  bringing  on 
dilatation  quicken  the  pulse- 
rate,  and  an  enlarged  but  slowly 
beating  heart  is  almost  always 
hypertrophied.  In  hypertrophy 
of  the  left  ventricle,  in  contra- 
distinction to  that  of  the  right, 
the  maximum  impulse  is  usually 
a  systolic  protrusion,  while  in 
the  latter  case  it  is  a  systolic 
retraction.  The  latter  is  also 
frequently  the  case  when  both 
ventricles  are  hypertrophied. 

Hypertrophy  of  the  Left  Ven= 
tricle.  —  Palpation  of  the  apex 
impulse,  which  many  writers, 
even  as  late  as  Romberg,  con- 
sider a  most  important  sign  of  hypertrophy  of  the  left  ventricle,  need  not 
be  decisive,  since,  as  Katzenstein  has  shown,  the  weakest  hearts  may  often 
beat  the  most  violently,  especially  when  beating  rapidly;  the  strongest,  on 
the  other  hand,  may  be  separated  from  the  chest  wall  by  a  layer  of  lung. 
Dulness  is,  however,  increased  to  the  left. 

Hypertrophy  of  the  Right  Ventricle. —  The  hypertrophy  of  the  right 
ventricle  is  not  so  easy  to  diagnose.  Its  presence  may  be  inferred  when 
the  area  of  cardiac  dulness  is  enlarged  and  a  systolic  retraction  is 

14 


Fig.  139. — Areas  of  pulsation  and  retraction  hyper- 
trophy of  the  right  and  left  ventricles.  ^,  retraction; 
""■,  pulsation.  Tlie  light  line  indicates  the  area  of  the 
cardiac  dulness.  A.  Hypertrophy  of  the  left  ventricle. 
B.   Hypertrophy  of  the  right  ventricle. 


210  DISEASES   OF   THE   HEART   AND    AORTA. 

noted  at  the  point  of  maximal  impulse  and  over  the  interspaces  between 
it  and  the  sternum  as  well  as  in  the  epigastrium.  The  heart  need  not  be 
enlarged  toward  the  right,  since  the  right  ventricle  rarely  passes  the  sternal 
margin.  Indeed  it  rather  tends  to  lift  the  apex  and  shift  it  to  the  left.  The 
area  of  cardiac  flatness  is  increased  to  the  right,  reaching 
to  the  sternal  margin.  An  increased  area  of  dulness  to  the  right  of  the  ster- 
num is  due  to  the  right  auricle.  The  second  pulmonic  sound  is  intensified 
and  ringing,  but  this  may  also  be  the  case  in  any  condition  in  which  there 
is  some  obstruction  to  the  pulmonary  circulation  or  some  insufficiency  of 
the  left  heart. 

Hypertrophy  of  the  auricles  cannot  be  diagnosed  from 
objective  signs  except  in  mitral  stenosis,  in  which  an  hypertrophied  auricle 
gives  rise  to  a  loud  presystolic  murmur.  This  is  not  present  when  the  auri- 
cle is  weak.  Hypertrophy  of  the  right  auricle  is  sometimes  shown  by  a 
high  presystolic  wave  upon  the  jugular  venous  pulse-curve  and  very  rarely 
by  a  presystolic  wave  upon  the  liver  pulse  (Mackenzie) ;  but,  as  a  rule,  it 
shows  no  signs. 

Prognosis. — A  certain  amount  of  hypertrophy  is  necessary  whenever 
a  valvular  lesion  or  any  other  abnormal  factor  tending  to  increase  the 
work  of  maintaining  the  circulation  is  present.  Hence  failure  of  the  heart 
to  hypertrophy  under  these  conditions  would  be  regarded  as  an  unfavor- 
able condition,  and  would  probably  soon  be  associated  with  cachexia.  On 
the  other  hand,  an  extreme  degree  of  hypertrophy  is  evidence  that  the 
heart  is  doing  its  maximal  work,  that  the  fibres  ere  long  will  begin  to 
degenerate,  and  the  heart  must  be  spared  as  much  as  possible. 

Hypertrophy  in  itself  does  not  demand  treatment,  but  diminution  of 
the  causal  factor  as  far  as  is  possible  is  advisable.  If  this  be  nephritis  or 
arteriosclerosis,  a  quiet  life  and  diet  poor  in  salt  and  purin  bodies  should 
be  resorted  to,  with  occasional  courses  of  potassium  iodide.  If  a  valvular 
lesion  be  present  and  the  hypertrophy  is  slight,  little  attention  need  be 
paid  to  it  until  the  patient  reaches  the  latter  half  of  the  fourth  decade, 
when  he  should  begin  to  spare  his  heart  and  arteries  as  much  as  possible, 
should  abstain  from  alcohol,  coffee,  and  tobacco,  and  should  in  every  way 
avoid  those  influences  leading  to  the  production  of  high  blood-pressure  and 
arteriosclerosis. 

Reserve  Force  of  the  Hypertrophied  Heart. — One  of  the  most  impor- 
tant questions  that  arise  in  connection  with  hypertrophied  hearts  is 
whether  or  not  a  hypertrophied  heart  possesses  as  much  reserve  force  as  a 
normal  one.  This  question  is  variously  answered  in  the  text-books,  most 
of  them  agreeing  with  Krehl  et  al.  that  the  reserve  force  is  lessened;  while 
the  experimental  work,  especially  that  of  Romberg  and  Hasenfeld,  indi- 
cates that  the  strength  of  the  hypertrophied  heart  muscle  itself  is  actually 
increased.  However,  a  great  deal  depends  upon  the  stage  of  hypertrophy 
in  which  the  individual  heart  happens  to  be.  Thus  a  heart  in  the  first 
stage,  with  fibres  normal  and  hypertrophied,  would  show  an  increased 
strength  (as  in  athletes'  hearts,  or  in  hearts  of  early  hypertrophy  after 
valvular  lesion  as  compared  to  the  same  hearts  at  the  very  onset  of  the 
lesion) ;  while  a  heart  in  the  second  stage,  with  fibres  partly  hypertrophic, 
partly   atrophic,   would   in    most   cases    show    a    marked    diminution    in 


HYPERTROPHY  AND  ATROPHY. 


211 


strength  and  still  greater  loss  in  reserve  force,  and  an  increased  effort  would 
hasten  the  degeneration. 

Another  and  really  main  factor  in  the  apparent  weakness  of  the  hyper- 
trophied  heart  is  that  in  practically  all  hearts  the  hypertrophy  is  brought 
on  by  some  valvular  lesion  or  by  some  persistent  increase  in  peripheral 
resistance ;  so  that  such  hearts  are  continually  wasting  much  of  their  energy 
in  overcoming  these  pathological  conditions,  besides  bestowing  the  usual 
amount  of  it  upon  the  maintenance  of  the  circulation.  In  bodily  exertion 
or  other  conditions  calling  upon  the  reserve  force,  not  only  the  actual 
circulation  must  be  increased,  but  the  abnormal  factor 
inducing  wasting,  of  energy,  the  valvular  lesion,  etc.,  « 

becomes  more  severe  as  well,  and  hence  the  extra  call  i         S  * 

upon  the  diseased  heart  is  double  the  extra  call  upon  the 
normal  and  requires  double  the  reserve  force  to  meet  it. 
Otherwise  the  reserve  force,  though  actually  more,  may 
be  apparently  less  than  in  the  normal  heart,  as  shown 
diagrammatically  in  Fig.  140.  For  practical  purposes, 
however,  it  may  be  regarded  as  indisputable  that,  in 
every  case  where  a  cardiac  lesion  is  present,  the  hyper- 
trophied  heart  has  less  available  reserve  force  than 
normally,  and  in  some  cases  (stage  3)  less  than  if  it 
had  not  hypertrophied  at  all. 


ATROPHY. 


Fig.  140. — Diagram 
showing  power  of  nor- 
mal and  hypertrophied 
(athlete's)  heart  at  rest 
and  during  exercise,  also 
that  of  a  diseased  heart. 
The  length  of  the  arrow 
indicates  the  reserve 
force.  The  unshaded 
portion  indicates  the 
cardiac  energy  ex- 
pended, but  wastedi 
owing  to  the  lesion. 


Atrophy  of  the  heart  is  more  or  less  the  reverse 
process  of  hypertrophy.  Whenever  the  body  diminishes 
in  weight  from  cachexia,  infectious  disease,  or  starva- 
tion, the  heart  muscle  diminishes  with  it,  and  according 
to  Hirsch  in  about  the  same  ratio.  The  epicardial  fat, 
on  the  other  hand,  is  but  little  diminished.  When  the 
atrophy  is  the  result  of  starvation  it  may  be  of  very 
high  degree,  but  the  size  and  condition  of  the  heart  may  return  to  normal 
when  an  adequate  diet  is  resumed  (Schieffer). 

As  in  the  case  of  hypertrophy,  there  seems  to  be  little  change  in  the 
number  of  the  muscle-cells,  but  the  latter  diminish  in  size  (10.84  //  instead 
of  12.85  n,  Goldenberg),  and  the  removal  of  substance  is  marked  by  the 
deposition  of  brown  granules  of  hsematoidin  in  fusiform  arrangement  about 
the  nucleus.  These  granules  are  formed  when  part  of  the  muscle-cell  pro- 
teid  is  broken  down  during  the  atrophy,  the  haematoidin  portion  being 
left.  Macroscopically  they  impart  a  tobacco-brown  color  to  the  heart,  so 
that  the  condition  is  often  designated  as  "brown  atrophy  of  the  heart." 

To  a  certain  extent  a  diminution  in  size  of  any  chamber  of  the  heart 
may  occur  if  its  work  is  lessened  by  obstruction  to  the  blood  flowing  into 
it;  as,  for  example,  the  left  ventricle  in  pure  uncomplicated  mitral  stenosis. 
The  atrophy  is  rarely  so  marked  here  as  in  starvation,  phthisis,  or  cachexia, 
and  is  indeed  the  exception  rather  than  the  rule  in  mitral  stenosis,  for  other 
factors,  tachycardia,  irregularity,  or  mitral  insufficiency,  usually  contrib- 
ute to  keep  the  left  ventricle  doing  an  at  least  normal  amount  of  work. 


212  DISEASES   OF  THE   HEART   AND    AORTA. 

Like  hypertrophy,  caehexial  atrophy  of  the  fibres  may  lead  on  to  growth 
of  interstitial  connective  tissue  and  fibrous  myocarditis,  but  true  brown 
atrophy  is  not  so  common  a  forerunner  of  myocarditis  as  is  hypertrophy 
of  the  heart.  Functionally,  the  force  of  the  heart  is  impaired  about  propor- 
tionally to  its  diminution  in  weight.  The  blood-pressure  is  usually  low 
and  the  muscle  easily  fatigued.  Overstrain  readily  occurs  in  such  hearts; 
and  sudden  death  is  not  uncommon. 

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Joseph,  D.  R.:  The  Ratio  between  the  Heart-weight  and  Body-weight  in  Various  Animals, 

J,  Exper.  Med.,  N.  York  and  Lancaster,  1908,  x,  521. 
Schieffer:    Ueber    den  Einfluss  der  Berufsarbeit  auf  die  Herzgrosse,  Deutsch.  Arch.  f. 

klin.  Med.,  Leipz.,  1908,  xcii,  383;  also,  Ueber  den  Einfluss  des  Militardienstes  auf  die 

Herzgrosse,  ibid.,  1908,  xcii,  392. 
Howard,  W,  T.:  An  Analysis  of  105  Cases  of  Heart  Hypertrophy  (from  the  Autopsy 

Records  of  the  Johns  Hopkins  Hospital),  Johns  Hopkins  Hosp.  Rep.,  Bait.,  1894, 

iii,  266. 
Wilks,  S.:  Ca.scs  of  Bright's  Disease,  with  Remarks,  Guy's  Hosp.  Rep.,  Lond,,  1853,  ii 

Ser.,  viii,  232. 


HYPERTROPHY  AND  ATROPHY.  213 

Senator,  H.:  Ueber  die  Herzhypertrophie  bei  Nierenkranken,  Deutsch.  med.  Wchnschr., 

Leipz.  u.  Wien,  1903.     Die  Erkrankungen  der  Niere,  Nothnagel's  Handb.  d.  speziellen 

Pathol,  u.  Th.,  Wien. 
Passler,  H.:  Ueber  Ursache  und  Beutung  der  Herzaffektion  Nierenkranker,  Volkmann's 

Sanunlung  klin.  Vortrage,  Leipz.,   1906,  No.  408. 
Johnson,  G.:  Lectures  on  Bright's  Disease  with  Especial  Reference  to  Pathology,  Diag- 
nosis, and  Treatment,  Lond.,  1873. 
Cohnheim,  J.:  Lectures  on  General  Pathology,  New  Sydenham  Society. 
Traube,  L.:  Gesammelte  Beitrage  zur  Pathologie  und  Physiologie,  Berl.,  1871-1878. 
Buhl:  Mitth.  a.  d.  pathol.  Inst.  Munchen,  1878,  38. 
Huchard,  H.:  Maladies  du  Coeur,  Paris,  1899-1905. 
Albrecht,  E.:  Der  Herzmuskel,  Berl.,  1903. 
Josu6  O.;  Hvpertrophie  cardiaque  causee  per  I'adrenahne,  Compt.  rend.  Soc.  de  Biol., 

Par.,  1907,  Ixiii,  285. 
Erb,  W.:  Experimentelle  und  histologische  Studien  iiber  Arterienerkrankung  nach  Adre- 

nalininjektionen,  Arch.  f.  exper.  Pathol,  u.  Pharmakol.,  Leipz.,  1905,  liii,  173. 
Vaquez:  Hypertension  arterielle.  Bull.  soc.  med.  d.  hop.  de  Paris,  Feb.  5,  1904. 
Vaquez   and   Aubertin:  Sur  I'hyperplasie   surr^nale   des   nephrites   hypertensives,   ibid., 

1905,  xxii,  705. 
Wiesel:  Renale  Herzhypertrophie  und  chromaffines  System,  Wien.  med.  Wchnschr.,  1907, 

Ivii,  673. 
Schur,  H.,  and  Wiesel,  J.:    Beitrage  zur  Physiologie  und  Pathologie  des  chromafiinen 

Gewebes,  Wien.  klin.  Wchnschr.,  1907,  xx,  1202.     Also,  Ueber  eine  der  Adrenalin- 

wirkung  analoge  Wirkung  des  Blutserums  von  Nephritikern  auf  das  Froschauge,  Wien. 

klin.  Wchnschr.,  1901,  xx,  699. 
Gaillard.     Quoted  from  Aubertin. 
Hasenfeld,  A.:  Ueber  die  Entwicklung  einer  Herzhypertrophie  bei  der  Pyocyaneusendo- 

carditis  und  der  dadurch  verursachten  Allgemeininfection,  Deutsch.  Arch.  f.  klin. 

Med.,  Leipz.,   1899,  Ixiv,  763. 
Hasenfeld  und   Romberg:  Ueber  die  Reservekraft  des  hypertrophischen  Herzmuskels, 

u.  s.  w..  Arch.  f.  exper.  Pathol,  u.  Pharmakol.,  1897,  xxxix,  333. 
Katzenstein,  J.:  Dilatation  und  Hypertrophie  des  Herzens,  Muenchen,  1903. 
Aschoff  and  Cohn:  Bemerkungen  zu  der  Schur- Wieselschen  Lehre  von  der  Hypertrophie 

des  Nebernierenmarkes  bei  chronischen  Erkrankungen  der  Nieren  und  des  Gefass- 

apparatus,  Verhandl.  d.  deutsch.  path.  Gesellsch.,  Jena,  1908,  xii,  131. 


VIII. 

FATTY  DEPOSITS  IN  AND  ABOUT  THE  HEART. 

Fat  may  be  deposited  in  the  heart  in  two  ways:  (1)  In  solid  masses 
of  adipose  tissue,  especially  in  the  pericardium  in  fat  individuals,  particu- 
larly in  those  addicted  to  alcohol,  and  very  often  associated  with  coronary 
sclerosis.   This  condition  is  designated  as  fatty  infiltration  or  obese 


Fig.  141. — Distribution  of  fat  in  and  about  the  heart.    A,  normal;  B,  deposit  in  an  obese  heart;  C,  deposit 

in  a  fatty  degenerated  heart. 

heart  (Mastfettherz,  Kisch).  (2)  In  fine  droplets  occurring  diffusely 
within  the  heart  muscle-cells,  especially  in  anaemia,  infectious  diseases,  in 
persons  poisoned  by  phosphorus,  arsenic,  and  numerous  other  substances, 
and  in  association  with  other  changes  in  the  myocardium.  This  condition 
is  called    fatty    degeneration. 

FATTY   INFILTRATION   OR    OBESITY    OF    THE   HEART. 

DEPOSITION    OF    THE    FAT. 

Harvey,  the  discoverer  of  the  circulation,  describes  the  hearts  of  certain 
fat  persons  as  covered  with  a  layer  of  fat  so  extensive  as  almost  to  obscure 
the  heart  muscle  from  view,  and  this  condition  is  one  of  not  very  infrequent 
occurrence.  In  normal  hearts  there  is  a  considerable  amount  of  fat  (30 
to  60  Gm.,  1  to  2  ounces)  collected  just  beneath  the  endothelial  layer  of  the 
pericardium,  along  the  auriculoventricular  and  interventricular  grooves 
(coronary  and  longitudinal  sulci),  at  the  base  of  the  aorta,  and  scattered 
elsewhere  over  the  heart.  As  the  individual  lays  on  more  body  fat,  more 
fat  is  deposited  in  the  pericardium,  at  first  only  at  the  usual  sites  along  the 
sulci;  but  later  it  spreads  over  and  into  the  myocardium,  penetrating  into 
it  between  the  larger  strands  of  muscle,  and  finally  settling  beneath  the 
endocardium,  especially  about  the  bases  of  the  papillary  muscles. 

The  weight  of  adipose  tissue  may  actually  exceed  the  weight  of  cardiac  muscle 
(W.  Miiller,  Hirsch,  Kisch),  as  shown  by  the  following  figures  determined  by  W.  Miiller 
(for  the  method  see  page  4). 
214 


FATTY  DEPOSITS  IN  AND  ABOUT  THE  HEART. 


215 


Total  weight 
of  heart. 


253.6 
363.5 
327.6 
494.3 


Heart 
muscle. 


240.7 
326.2 
181.3 
228.3 


Fat  removable  by 
dissection. 


12.9 
37.3 

146.3 

266 


Per  cent, 
of  fat. 


5.1 
10.3 
45.6 
53.5 


Normal  male  (thin). 
Cardiac  hypertrophy. 


Nature  of  the  Fatty  Deposit. — Under  these  circumstances  the  fat  is  deposited  in 
exactly  the  same  manner  as  elsewhere  in  the  body.  The  pathological  character  con- 
sists not  in  the  process  but  in  the  amount  of  the  deposit.  The  adipose  tissue  in  this 
region  does  not  differ  macroscopically  or  microscopically  from  the  fat  elsewhere.  Neither 
does  it  differ  chemically.     It  is  ordinary  "  translocation  fat"  (Rosenfeld,  Leick  and 


Fig.  142. — Photomicrographs  of  fat  deposits  in  the  heart.  A.  Heart  muscle  of  an  obese  indi- 
vidual, showing  fat  cells.  B.  Heart  muscle  of  a  patient  who  died  of  pneumonia,  showing  fat  droplets 
within  the  cells  (fatty  degeneration).     (Photomicrograph  by  Dr.  Clias.  S.  Bond.) 

Winckler),  derived  directly  from  the  food;  for  Leick  and  Winckler  have  shown  that  if 
dogs  be  overfed  with  mutton  tallow,  the  fat  deposited  in  the  pericardium  has  an  iodine 
absorption  coefficient  approaching  more  nearly  to  what  is  in  the  sheep  than  to  that  of  the 
dog.  The  pericardial  fat  differs  from  the  fat  elsewhere  in  but  one  important  respect,  and 
one  which  is  especially  to  be  borne  in  mind  in  treating  the  condition,  namely,  that  it  is 
relatively  poor  in  lipase,  the  enzyme  which  forms  and  splits  fat,  and  hence  is 
relatively  stable.  According  to  Loevenhart  it  would  appear  that  lipase  is  present 
in  the  cells  in  considerable  amounts  at  the  time  the  fat  is  deposited,  but  is  then  gradually 
destroyed;  so  that  if  subsequently  the  fat  of  the  body  is  reduced  from  inanition  or  other 
cause,  there  is  no  more  enzyme  remaining  in  the  pericardium  to  split  up  what  is  stored 
there  and  to  return  it  to  the  general  circulation.  Accordingly,  it  is  found  that  in  starva- 
tion the  pericardial  and  perirenal  fat  remain  after  all  the  rest  has 
disappeared  from  the  body  (Loevenhart,  Schieffer).  This  matter  will  be  re- 
ferred to  again  in  connection  with  treatment. 


216 


DISEASES   OF   THE    HEART    AND    AORTA. 


CARDIAC    CONDITIONS    ASSOCIATED    WITH    OBESITY. 

There  are  three  definite  conditions  which,  though  in  no  way  part  of 
the  general  process  of  obesity,  are  often  associated  with  it;  and  it  is 
these,  rather  than  the  obesity  itself,  which  give  rise  to 
the    symptom    complex    referred   to    as  "fatty  heart,"  or,  as 

Romberg  more  properly  designates 
it,  "cardiac  insufficiency  of  fat  per- 
sons "  (Die  Herzmuskelinsufficienz 
der  Fettleibingen) .  These  are  (1) 
atrophy  of  the  heart  muscle,  and 
(2)  s  c  1  e  r  o  s  i  s  of  the  coronary  arte- 
ries,  (3)  a  high  diaphragm. 

1.  Atrophy  and  Cardiosclerosis. 
— It  is  especially  worthy  of  notice 
that  the  increase  in  size  and  weight 
of  the  heart  may  conceal  an  actual 
atrophy  of  the  heart  muscle  (Hirsch) 
(see  table  above)  and  a  correspond- 
ing weakness  of  the  heart.  Accord- 
ing to  most  writers,  this  lies  mainly 
in  the  left  ventricle,  but  Hirsch  has 
shown  that  not  only  does  the  fatty 
infiltration  penetrate  chiefly 
the  wall  of  the  right  ventricle,  but 
that  the  symptoms  most  common 
among  fat  persons  are  those  due  to 
primary  failure  of  the  right 
side  of  the  heart.  A  general  cardio- 
sclerosis (see  page  235)  is  often  asso- 
ciated with- the  deposit  of  fat.  It  is  a 
self-evident  fact  that  such  enormous 
deposits  of  fat  increase  the  work 
done  by  the  heart,  first  by  increas- 
ing the  weight  to  be  moved  at  each 
systole,  and  secondly  by  increasing 
the  total  bed  of  the  blood  stream. 
It  might  be  supposed  that  this  would 
in  itself  bring  about  hypertrophy,  but  hypertrophy  is  rarely  demonstrable. 
The  tendency  to  obesity  usually  occurs  either  in  persons  whose  lives  are 
sedentary  and  whose  skeletal  and  cardiac  muscles  are  therefore  under- 
developed, or  else  in  those  addicted  to  excesses  of  alcohol  or  overeating, 
factors  which  in  themselves  bring  on  myocardial  changes  and  hypertrophy. 

2.  Coronary  Sclerosis. —  The  pathological  changes  and  symptoms  due 
to  sclerosis  of  the  coronary  arteries  do  not  differ  from  those  arising  without 
the  presence  of  abnormal  fat  deposits  and  will  be  discussed  in  a  separate 
chapter  (page  280). 

3.  High  Diaphragm. — \.  Frey  and  Krehl  have  shown  in  animals  that 
pushing  up  the  diaphragm,  and  thus  displacing  the  heart,  greatly  inter- 


FiG.  143. — An  excessive  deposit  of  epicardial 
fat.  (From  a  specimen  in  the  Army  Medical  Mu- 
seum, Washington,  D.  C.) 


FATTY  DEPOSITS  IN  AND  ABOUT  THE  HEART.  217 

feres  with  the  work  of  the  latter.  Myers  and  Schott  found  that  soldiers 
whose  diaphragms  are  pushed  up  by  tight  belts  about  the  abdomen  exhibit 
symptoms  of  cardiac  overstrain  much  more  readily  than  do  normal  indi- 
viduals. Myers  found  acute  dilatations  most  common  in  the  British 
regiments  in  which  cuirasses  and  tight  belts  were  worn. 

Wenckebach  has  called  attention  to  the  fact  that  a  large  amount 
of  intra-abdominal  fat  pushes  up  the  diaphragm  and  thus  pushes  the 
heart  into  a  more  transverse  position  (apex  often  in  the  fourth  interspace), 
thereby  hampering  its  action.  This  factor  must  be  reckoned  with  in  the 
genesis  of  the  cardiac  weakness  of  fat  persons. 

ETIOLOGY. 

Clinically,  the  cardiac  manifestations  in  fat  persons  are  very  variable. 
They  occur  most  frequently  in  association  with  (1)  general  obesity,  either 
hereditary  or  arising  primarily  from  over-eating;  (2)  in  childhood;  (3)  after 
castration  or  menopause;  (4)  overindulgence  in  alcohol,  especially  malt 
liquors,  with  or  without  the  presence  of  gout;  (5)  diabetes  mellitus  with 
obesity  (lipogenous  diabetes) ;  (6)  they  are  most  frequent  and  most  intense 
after  the  age  of  fifty. 

PHYSICAL    SIGNS. 

Upon  physical  examination  the  most  striking  features  are  the  general 
obesity;  the  relative  weakness  of  the  skeletal  muscles;  the  groups  of  dilated 
venules,  especially  the  "Bardolphian"  "butterfly"  area  of  dilated  venules 
about  nose  and  cheeks,  as  well  as  similar  areas  along  the  attachment  of 
the  diaphragm  and  elsewhere.  According  to  Hirsch,  dilatation  of  the 
superficial  veins  in  the  subcutaneous  fat  is  a  premonitory  sign  of  cardiac 
weakening;  but  this  is  certainly  not  the  case  always.  Often  there  is  no 
visible  apex  impulse;  the  relative  cardiac  dulness  is  increased  to  both  left 
and  right,  owing  to  the  transverse  position;  the  cardiac  flatness  is  dimin- 
ished. The  heart  sounds  usually  have  a  distant  character  and  may  be  free 
from  murmurs.  Occasionally  there  may  be  slight  oedema  of  the  feet  and  a 
small  amount  of  albumin  in  the  urine.  In  advanced  cases  of  cardiac  insuf- 
ficiency the  patient  may  become  much  thinner  (owing  to  diminished  absorp- 
tion of  fat  from  the  intestine,  see  page  159),  but  the  pericardial  fat  may 
remain  undiminished. 

TREATMENT. 

The  treatment  of  cardiac  weakness  of  fat  persons  depends  entirely  upon 
the  stage  at  which  the  patient  is  seen.  If  oedema  and  persistent  dyspnoea  or 
palpitation  upon  slight  exertion  are  already  present,  the  case  must  be  treated 
exactly  like  one  of  cardiac  overstrain  or  heart  failure  from  any  other  cause 
manifesting  similar  symptoms,  except  that,  owing  to  the  frequent  atrophy 
and  infiltration  of  the  heart  muscle,  drugs  of  the  digitalis  group  are  often 
of  little  use  and  may  even  be  harmful.  The  patient  should  be  put  upon  rest, 
restricted  diet,  with  liquids  restricted  to  1000  c.c,  purged  freely,  and 
bled  if  symptoms  of  failure  of  the  right  heart  set  in.  Amyl  nitrite,  nitro- 
glycerin, and  erythrol  tetranitrate  may  be  used  to  relieve  attacks  of  dysp- 
noea, and  massage,  passive  movements,  and  finally  resisted  movements,  and 
cold  water  or  Nauheim  baths  when  the  patient  is  able  to  get  out  of  bed. 


218 


DISEASES   OF  THE    HEART   AND   AORTA. 


When,  as  is  usually  the  case,  the  patient  is  seen  before  the  stage  of 
actual  heart  failure  has  set  in  and  is  suffering  only  from  what  may  be  con- 
sidered as  the  premonitory  symptoms  of  cardiac  affection, — palpitation 
and  shortness  of  breath  on  exertion,  weakness,  and  giddiness, — the  treat- 
ment should  then  be  directed  toward  the  obesity  rather  than  toward  the 
heart.  A  main  indication  is  then  gradually  to  restrict  the  diet  to  a  heat 
equivalent  of  about  1200  to  1700  calories,  of  which  500  calories  (about  120 
Gm.,  4  oz.)  should  be  proteid  (v.  Noorden). 

(1)  Restricted  Diet. — Numerous  restricted  diets  have  been  laid  down, 
especially  by  Banting,  Oertel,  Hirschfeld,  Kisch,  and  Ebstein.  The  restric- 
tion should  not  take  place  suddenly,  for  fear  of  weakening  the  patient,  but 
should  take  place  in  several  stages,  reducing  500  calories  each  week  until 
the  lower  limit  is  reached.* 

(2)  Liquids  should  be  restricted  to  less  than  1000  c.c.  (1  quart)  per 
day;  this  also  should  be  done  gradually.^ 

Sample  Diet. — V.  Noorden  gives  the  following  outline  diet,  which  is  very  satisfactory 
as  a  basis  capable  of  modification: 


Prot. 


8  A.M. 


Breakfast — 

80  Gm.  cold  lean  meat 

i  white  roll  (25  Gm.) 

1  egg 

1  cup  lean  bouillon 

I  f  1  small  plate  clear  soup 

'  I  150  Gm.  (5  oz.)  lean  meat  or  fish. . . . 

1  P.M.  {  100  Gm.  potatoes 

I  I  Peas,  beans,  cauliflower,  asparagus 

1 100  Gm.  fresh  fruit 

Black  coffee 

200  Gm.  fresh  fruit 

250  c.c  (1  glass)  skim-milk 

Supper — 

125  Gm.  cold  lean  meat  with  pickles. 

Red  beets,  radishes,  etc 

30  Gm.  graham  bread 


10  A.M. 

12  m. 


3p.m 

4  P.M. 

6  p.m. 
8  p.m. 


2-3  teaspoonf uls  boiled  fruit  (no  sugar) . , 


Total. 


30.5 
1.8 
6.5 

0.8 
57.3 
1.9 
3.0 
0.5 

6 
6.8 

36 
2 

2.0 
0.5 


1556 


Fat. 


1.4 
0.2 
6.1 
0.8 
2.0 
2.8 

10 


2.0 
3 
0.3 


Carb. 


14 


180 

15 

8 

16 
12 


5 
12 

8 


28.6 


112 


Cal. 


205 

85 

7 


583 

0 

90 

97 


299 


1087 


*  100  Gm.  (3  oz.)  raw  meat  (proteid  20  per  cent.,  fat  1.7  per  cent.)  =  100  cal.  100  Gm. 
(3  oz.)  cooked  lean  meat  (proteid  37  per  cent.,  fat  2.5  per  cent.)  =  175  cal.  (about  25  per 
cent,  higher  in  well-done  roasted  meats).  100  Gm.  (3  oz.)  cooked  meat  of  stall-fed  animals 
(no  visible  fat)  (proteid  36  per  cent.,  fat  6  per  cent.)  =  200  cal.  1  egg  (6.5  Gm.  proteid  + 
6:2  Gm.  fat)  =  85  cal.  Cheese  (proteid  28  per  cent.,  fat  30  per  cent.,  carbohydrate  2  per 
cent.)  =400  cal.  Milk  (proteid  3.4  per  cent.,  fat  3.0  per  cent.,  sugar  4.5  per  cent.)  =  60  cal. 
per  100  c.c.  (20  cal.  per  ounce).  Potatoes  100  Gm.  (3  oz.)=80  cal.  Bread  (proteid  7-9 
per  cent.,  carbohydrate  35  to  80  per  cent.,  the  latter  in  zwieback  and  dry  breads)  100  Gm.  = 
200-350  cal.     Sugar  100  Gm.  =  400  cal.     Butter  100  Gm.  =  930  cal. 

'  Oert«l  and  Schweninger  thought  that  drinking  water  is  a  factor  producing  fat. 
Straub  and  others  have  shown  that  this  is  by  no  means  the  case.  The  only  influence  of 
the  water  lies  in  the  fact  that  when  a  meal  is  taken  dry  the  appetite  is  less  than  when  water 
is  taken,  and  consequently  less  is  eaten.  However,  considerable  amounts  of  fluid  increase 
the  volume  of  blood  and  the  work  of  the  heart,  and  hence  the  limitation  of  fluid  saves 
the  heart  in  this  way. 


FATTY  DEPOSITS  IN  AND  ABOUT  THE  HEART. 


219 


(3)  Increased  Exercise. — Increase  exercise  gradually  as  much  as  pos- 
sible, especially  by  walking,  either  on  the  level  or  on  gentle  gradual  ascents, 
interrupted  by  frequent  rests  before  either  weariness  or  shortness  of  breath 
sets  in,'  In  this  way  the  energy  used  by  the  body,  and  hence  also  the  fat 
burned  up,  can  be  materially  increased. 


Weight  of  patient 

Rate  2.7  miles  per  hour. 
Rate  3.4  miles  per  hour . 


Per  mile. 

150  lbs. 
60  cal. 
75  cal. 

200  lbs. 

85  cal. 

100  cal. 

Walking  on  Level. 


Per  hour. 


150  lbs. 
170  cal.  (18  Gm.  fat) 
230  cal.  (30  Gm.  fat) 


200  lbs. 
225  cal.  (25  Gm.  fat) 
310  cal.  (40  Gm.  fat) 


In  walking  up  grade  the  energy  used  up  is  equal  to  elevation  X  weight  of  patient 
plus  the  energy  expended  in  traversing  the  distance;  but  this  is  theoretically  equalled 
by  the  energy  saved  in  the  subsequent  descent,  and,  on  the  other  hand,  both  are 
increased  by  bringing  into  play  a  different  group  of  muscles;  these  factors  can  scarcely 
even  be  approximately  estimated  in  the  individual  case.  However,  Zuntz  gives  the  fol- 
lowing empirical  figures:  a  man,  150  lbs.,  climbing  3  kilometres  (1.8  miles)  in  one  hour 
upon  a  10  per  cent,  grade  uses  up  about  28  Gm.  (almost  1  ounce)  of  fat. 

(4)  Resisted  movements  (Schott)  carried  out  under  the  supervision  of 
an  attendant;  or  contraction  of  antagonistic  muscles  (Herz)  (see  page  194). 

(5)  Nauheim  baths  (see  page  201)  or  daily  cold  baths  as  cold  as  can 
be  borne  by  the  patient  without  shock. 

(6)  Drug  Treatment.  —  Strychnine  may  be  administered  to  increase 
muscular  tone,  provided  this  does  not  also  increase  the  appetite  too  much. 

Thyroid  extract  and  other  "antifat''  medication  should  be 
scrupulously  avoided.  Metabolism  experiments  have  shown  that  the  admin- 
istration of  thyroid  substance,  though  increasing  the  oxidative  processes,  causes  a  split- 
ting of  proteid  to  a  greater  degree  than  of  fat,  and  hence  defeats  its  own  end,  namely, 
that  of  burning  up  the  fat  without  affecting  the  muscle.  It  also  brings  about  palpita- 
tion, tachycardia,  and  other  distressing  symptoms,  and  tends  to  increase  rather  than  to 
diminish  the  cardiac  features,  even  though  it  may  be  diminishing  the  obesity  itself. 

In  the  obesity  of  the  menopause,  tablets  of  ovarian  extract  are 
used  to  increase  oxidation,  as  this  effect  has  been  demonstrated  in  animals, 
but  clinically  the  results  from  its  use  are  rather  uncertain. 

FATTY  DEGENERATION. 


— PATHOLOGY. 

Pathological  Anatomy. — In  the  condition  known  as  "fatty  degenera- 
tion" the  fat  is  deposited  not  by  an  increase  of  adipose  tissue  but  in  the 
form  of  fine  droplets  within  the  heart  muscle-cells  (Figs.  141  and  142). 

In  some  cases  these  droplets  can  be  seen  to  almost  fill  the  entire  cell, 
in  others  they  appear  as  a  few  diffusely  scattered  droplets  in  the  sarcoplasm. 

'  It  must  be  borne  in  mind  that  sclerosis  of  the  coronary  arteries  is  a  frequent  con- 
comitant of  heart  weakness  in  fat  people,  and  hence  sudden  overexertion  or  severe  exer- 
cises are  to  be  avoided,  at  least  until  the  physician  has  thoroughly  acquainted  himself  with 
the  patient's  condition  and  endurance. 


220  DISEASES   OF  THE    HEART    AND    AORTA. 

Not  all  the  cells  are  invaded  by  the  fat,  but  with  the  naked  eye  yellow  areas 
of  fatty  degeneration  may  be  seen  mingled  with  normal  areas  of  red-brown 
color,  which  appear  normal  in  structure  under  the  microscope. 

As  regards  distribution,  Ribbert  recognizes  three  types:  (1)  diffuse  general 
fatty  degeneration,  in  which  all  the  cells  are  loaded  with  fat;  (2)  mottled  de- 
generation, occurring  in  the  areas  which  lie  midway  between  or  at  points 
most  distant  from  the  larger  arteries;  occurring  especially  in  anaemic  individuals 
and  in  persons  whose  blood-pressure  is  very  low,  so  that  the  cells  which  are  most  distant 
from  the  arteries  suffer  from  ischa^mia;  (3)  mottled  periarterial  fatty  de- 
generation produced  by  the  action  of  poisonous  substances  in  the  circulating  blood,  such 
as  phosphorus,  arsenic,  bacterial  poisons,  etc.,  in  which  those  cells  suffer  most  which  are 
brought  most  closely  into  contact  with  the  poison,  i.e.,  the  cells  lying  in  the  vicinity  of  the 
larger  arteries,  while  the  areas  remote  from  these  vessels  are  normal  or  involved  to  a  lesser 
degree. 

Nature  of  Fatty  Degeneration.  —  The  fatty  degeneration  may  go  on 
in  hearts  otherwise  healthy  in  connection  with  infectious  diseases,  or  in 
chronic  myocarditis  and  in  valvular  heart  diseases.  The  exact  nature  of 
the  process  is  not  clear.  Virchow  termed  it  a  "degeneration,"  but  this 
term,  although  in  very  general  use,  does  not  seem  to  designate  accurately 
the  process.  It  appears  to  be  a  disturbance  of  cellular  metabolism  rather 
than  a  degeneration  of  cell  protoplasm,  and  it  has  been  suggested  that 
perhaps  this  is  due  to  some  interference  with  the  oxidizing  enzymes  such 
that  the  fat  cannot  be  oxidized,  just  as  the  sugar  fails  to  be  oxidized  in 
diabetes.     But  this  suggestion  is  not  founded  upon  any  experimental  data. 

It  is  therefore  most  important  from  the  stand-points  of  both  pathology 
and  prognosis  to  learn  where  this  fat  comes  from  and  how  it  is  formed. 
Virchow  was  the  first  to  teach  that  there  was  a  true  fatty  degeneration,  that 
is  that  the  fat  was  formed  from  non-fatty  (probably  proteid)  substances 
of  the  sarcoplasm.  It  must  be  borne  in  mind  that  the  fat  might  be  present 
in  combination  as  it  is  in  lecithin  without  being  visible,  but  that  it  may 
become  visible  when  it  is  split  off  from  the  lecithin  molecules  and  deposited 
as  highly  refractive  droplets  of  true  fat^ 

However,  the  analyses  of  numerous  observers  (Bottcher,  Krehl,  Rosenfeld)  show  a 
definite  increase  in  the  fat  present  in  the  heart  muscle  in  fatty  degeneration.  Indeed, 
according  to  Rosenfeld,  the  muscle  shows  "  fatty  degeneration  "  whenever  it  contains  more 
than  15-17  per  cent,  of  fat  within  the  muscle-cells  (in  marked  fatty  degeneration  usually 
20-21  per  cent.).  As  he  put  it,  ''there  is  no  true  fatty  degeneration,  but 
the  cell  becomes  poor  in  proteid  and  fat  enters  it."  That  this  fat  is 
not  derived  from  the  breaking  down  of  cell  substance,  but  is  derived  either  from 
the  fat  of  the  food  or  from  that  transferred  from  the  subcutaneous  tissue  else- 
where in  the  body,  has  been  shown  in  many  ways.  In  the  first  place,  Krehl  demonstrated 
that  the  lecithin  content  of  the  heart  muscle  was  practically  constant  and  quite  indepen- 
dent of  the  degree  of  fatty  degeneration,  and  hence  that  the  fat  was  not  derived  from  this 
source.  Secondly,  Rosenfeld  showed  that  in  a  heart  whose  left  ventricle  appeared  normal, 
but  whose  right  ventricle  was  very  yellow  in  appearance  (and  showed  fatty  degeneration 
on  section),  the  nature  of  the  fat  was  identical  in  both.  Thirdly,  it  was  shown  also  by  Rosen- 
feld that  if  dogs  were  starved  until  their  subcutaneous  fat  had  disappeared  and  were  then 
poisoned  with  phosphorus,  the  fatty  degeneration  did  not  then  appear  as  it  did  in  well- 
fed  dogs.  This  fact  was  further  demonstrated  by  Leick  and  Winckler,  who  poisoned  their 
dogs  with  phosphorus  and  then  fed  them  on  mutton  tallow  (iodine  absorption  coefficient 
38.2),  and  obtained  a  deposit  within  the  heart  muscle  not  of  dog  fat  (I.  A.  C.  58.6)  but  of 
mutton  tallow.  This  seems  to  prove  that  the  "fatty  degeneration"  of  heart  muscle  is 
simply  a  deposit  of  fat  within  the  muscle-cell,  just  as  it  occurs  within  the  connective-tissue 
cell  under  normal  circumstances.     The  deposition  of  this  fat  is  not  associated  with  any 


FATTY  DEPOSITS  IN  AND  ABOUT  THE  HEART.  221 

change  in  the  Hpase  of  the  heart  muscle  nor  of  the  Hver,  in  spite  of  the  apparent  increase 
in  fat  metabolism.  The  author  also  found  that  the  amount  of  lipase  in  the  lean  areas  of 
a  human  liver  mottled  with  fatty  degeneration  was  the  same  as  in  the  neighboring  yellow 
areas.  It  would  appear,  therefore,  that,  chemically,  the  primary  change  being  absent,  fatty 
degeneration  lies  not  in  the  heart  but  elsewhere  in  the  body.  This  is  further  borne  out  by 
the  fact  that  in  animals  poisoned  with  phosphorus,  oil  of  pulegon,  etc.,  the  total  amount 
of  fat  in  the  body  is  diminished,  while  that  in  the  heart  and  liver  is  increased.  The  latter 
organs  seem  merely  to  deposit  the  fat  thrown  into  the  general  circulation. 

ETIOLOGY. 

Fatty  degeneration  in  the  human  heart  occurs  most  commonly  in 
association  with  alcohohsm,  either  acute  or  chronic,  primary  and  secondary 
anaemias,  after  hemorrhages,  in  association  with  myocarditis,  valvular 
and  other  cardiac  lesions,  in  most  infectious  diseases,  in  miners,  smelters, 
and  many  metal  workers,  as  well  as  in  numerous  other  industries  where 
poisonous  substances  are  employed.  In  a  number  of  cases  of  death 
from  chloroform  anesthesia  fatty  degeneration  has  been  found  and  is 
usually  ascribed  to  the  action  of  the  chloroform,  but  Rosenfeld  believes 
that  in  these  cases  the  fatty  degeneration  is  always  present  before  the 
chloroform  was  given,  and  that  this  fact  accounts  for  the  death  of  the 
patient. 

Not  infrequently,  as  in  cases  of  phosphorus  poisoning  and  of  infectious 
diseases,  the  same  agent  which  brings  about  the  fatty  degeneration  also 
gives  rise  to  diminished  tone  of  the  vasomotor  centre.  Failure  of  the  cir- 
culation may  result  from  the  latter  factor,  but  this  need  scarcely  be  ascribed 
to  the  fatty  change  in  the  heart. 

■   STRENGTH  OF  HEART  WITH  FATTY  DEGENERATION. 

These  results  of  cliemical  investigation  also  find  their  parallel  in  the 
effects  upon  muscle.  Welch,  in  1888,  was  able  to  show  that  the  hearts  of 
rabbits  rendered  fatty  by  prolonged  exposure  to  high  temperatures  were 
quite  normal  as  regards  preservation  of  blood-pressure,  reactions  to  vagus 
stimulation,  etc.;  while  Hasenfeld  and  Fenyvessy  ten  years  later  showed 
that  animals  poisoned  with  phosphorus  withstood  the  strain  from  clamping 
the  abdominal  aorta  quite  as  well  as  did  normal  animals.  On  the  other 
hand,  de  la  Camp  compelled  his  phosphorus  dogs  to  run  a  tread-mill  until 
fatigue  set  in,  and  found  with  the  X-ray  that  their  hearts  had  dilated, 
whereas  those  of  normal  dogs  did  not  dilate  under  these  circumstances. 
The  tonicity  of  the  cardiac  muscle  was  diminished. 
De  la  Camp's  experiments  have  not  been  repeated  as  yet,  but  they  seem 
to  have  been  very  carefully  carried  out.  It  seems  certain  that,  as  Kraus 
claims,  there  is  a  considerable  difference  between  the  endurance  of  normal 
hearts  and  of  those  with  fatty  degeneration. 

Moreover,  patients  with  fatty  degeneration  of  the  heart  are  very  sen- 
sitive to  digitalis  and  are  frequently  injured  by  it.  Sudden  death  from 
overdose  of  digitalis  or  from  acute  cardiac  overstrain  is  more  common  in 
patients  with  fatty  degeneration  of  the  heart  than  in  almost  any  other 
condition.  The  relative  frequency  with  which  fatty  degeneration  is  asso- 
ciated with  spontaneous  rupture  of  the  heart  is  also  evidence  of  weakness 
of  the  walls. 


222  DISEASES   OF   THE   HEART   AND    AORTA. 


SYMPTOMS    AND    SIGNS. 

The  most  characteristic  symptoms  associated  with  the  condition  are 
those  of  general  debility  and  feebleness,  more  or  less  languor  and  somno- 
lence, as  a  rule  without  marked  cardiorespiratory  symptoms  except  short- 
ness of  breath  on  exertion.  The  pulse  is  usually  small,  rather  collapsing, 
and  feeble;  the  blood-pressure  is  below  normal,  except  when  complicated 
by  chronic  myocarditis  or  valvular  lesion  (maximal  pressure  90  to  115 
mm.  Hg) ;  the  pulse-rate  is  increased.  On  physical  examination  the  heart 
may  be  either  normal  or  dilated,  the  sounds  either  feeble  and  distant  or 
short  and  sharp;  the  apex  impulse  may  or  may  not  be  well  marked.  The 
liver  and  spleen  are  often  enlarged  as  part  of  the  general  malady  of  which 
the  cardiac  condition  also  forms  a  part.  There  is  sometimes  oedema  of  the 
feet  and  ankles.  However,  it  must  be  frankly  admitted  that  none  of  these 
is  either  constant  or  characteristic;  and  the  diagnosis  may  have  to  be 
made  from  inference  only. 

DIAGNOSIS. 

The  diagnosis  of  fatty  degeneration  may  often  be  made  with  more  or 
less  probability  from  a  knowledge  of  the  etiological  factors,,  but  not  from 
any  of  the  physical  signs,  so  that,  as  Krehl  puts  it,  t  h  e  r  e  are  no  clin- 
ical signs  for  the  diagnosis  of  fatty  degeneration  of 
the   heart. 

TREATMENT. 

When  the  condition  is  recognized,  or  rather  suspected,  the  treatment 
consists  of  absolute  rest  in  bed  for  at  least  two  weeks  after  the  acute  dis- 
turbance has  passed  off  and  until  slowed  respiration  and  increased  tolerance 
to  mild  but  gradually  increasing  arm  exercises  show  that  the  heart  muscle 
has  regained  its  normal  condition.  Whether  it  is  possible  to  overcome  the 
fatty  degeneration  of  a  chronically  diseased  heart  is  questionable,  but  in 
that,  as  in  other  conditions,  treatment  must  be  guided  by  the  general 
response  of  the  patient,  and  over-exertion  must  constantly  be  shunned. 

It  must  be  borne  in  mind  that  hearts  which  are  in  a  state  of  fatty 
degeneration  are  particularly  sensitive  to  digitalis;  so  that,  when  this  con- 
dition is  suspected,  digitalis  should  be  either  avoided  or  given  in  smaller 
doses  than  usual. 

PROGNOSIS. 

Spontaneous  recovery  is  the  rule  if  too  great  a  burden  is  not  imposed 
on  the  heart;  but  in  spite  of  the  results  of  animal  experiments,  especially 
those  of  Welch  and  Hasenfeld  and  Fenyvessy,  attention  must  be  called 
to  the  fact  that  sudden  death  is  far  from  a  rare  occurrence  in  hearts  with 
fatty  degeneration.  It  occurs  most  frequently  after  or  during  exertion. 
One  can  scarcely  avoid  the  suspicion  that  perhaps  the  condition  which 
brings  about  the  change  in  the  fat  metabolism  is  also  one  which  limits  the 
total  metabolism  of  the  heart  muscle-cells  and  consequently  their  contrac- 
tility; so  that  after  a  certain  Umit  is  passed  they  suddenly  cease  their  func- 
tion, just  as  is  the  case  in  the  cellular  asphyxia  of  intermittent  claudica- 


FATTY  DEPOSITS  IN  AND  ABOUT  THE  HEART.  223 

tion  and  coronary  sclerosis  (see  page  282,  Fig.  166),  or  in  toxic  myocarditis 
from  diphtheria.  Spontaneous  rupture  of  the  heart  is  par- 
ticularly common  in  cases  of  fatty  degeneration.  The  latter  was  present 
in  77  per  cent,  of  the  cases  collected  by  Hamilton. 

BIBLIOGRAPHY. 

Heart  of  Obesity. 

Kisch,  H.:  Zur  Lehre  vom  Mastfettherzen,  Muenchen.  med.  Wchnschr.,  1902,  Hi,  546. 
Miiller,  W.:  Die  Massenverhaltnisse  des  menschlichen  Herzens,  Hamb.  u.  Leipz.,  1883. 
Hirsch,   K.:  Ueber  den  gegenwartigen  Stand  der  Lehre  vom  sogenannten  Fettherzen, 

Muenchen.  med.  Wchnschr.,  1901,  xlviii,  1867. 
Leick  and  Winckler:  Herkunft  des  Fettes  bei  Fettmetamorphose  des  Herzfleisches,  Arch. 

f.  exper.  Pathol,  u.  Pharmakol.,  Leipz.,  1902,  xlviii,  163. 
Loevenhart,  A.  S.:  On  the  Relation  of  Lipase  to  Fat  Metabolism — Lipogenesis,  Am.  J. 

Physiol.,  Host.,  1902,  vi,  331. 
Schieffer:  Ueber  den   Einfluss   des   Ernahrungszustandes   auf  die   Herzgrosse,  Deutsch. 

Arch.  f.  klin.  Med.,  Leipz.,  1908,  xcii,  54. 
Romberg,  E.:  Lehrbuch  der  Krankheiten  des  Herzens  und  der  Blutgefasse,  Stuttgart, 

1906. 
V.  Noorden,  K.:  Die  Fettsucht,  Nothnagel's  Spec.  Pathol,  u.  Therap.,  Vienna,  1900,  vol. 

vii,  1st  half. 
Banting,  W.:  Letter  on  Corpulence;  address  to  the  public,  1863,  1864,  1865,  1868. 
Oertel:    Kritisch-physiologische    Besprechung   der   Ebstein'schen    Behandlung  der  Fett- 

leibigkeit,  Leipz.,  1885.     Obesity,  Twentieth  Century  Practice  of  Med.,  N.  Y.,  1895. 
Hirschfeld:  Die  Behandlung  der  Fettleibigkeit,  Ztschr.  f.  klin.  Med.,  Berl.,  1893,  xxii,  142. 
Kisch:  Das  Mastfettherz,  Prag,  1894.     Zur  Insufficienz  des  Mastfettherzens,  Therap.  d. 

Gegenwart,  1899,  xl,  296. 
Ebstein,  W.:  Die  Fettliebigkeit  und  ihre  Behandlung,  Wiesbaden. 

Fatty  Degeneration  of  the  Heart. 

Ribbert,  H.:  Beitrage  zur  pathologischen  Anatomic  des  Herzens,  Arch.  f.  path.  Anat.  etc., 

Berl.,  1897,  cxlvii,  193. 
Krehl,  L.:  Ueber  fettige  Degeneration  des  Herzens,  Deutsch.  Arch.  f.  klin.  Med.,  Leipz., 

1893,  H,  1,  416. 
Rosenfeld,  G.:  Der  Prozess  der  Verfettung,  Berl.  klin.  Wchnschr.,  Berl.,  1904,  xli,  587. 

Ueber  Herzverfettung  beim  Menschen.,  Zentralbl.  f.  innere  Med.,  Leipz.,  1901,  xxii,  145. 
Leick  and  Winckler:  Herkunft  des  Fettes  bei  Fellmetamorphose  des  Herzfleisches,  Arch. 

f.  exper.  Pathol,  u.  Pharmakol.,  Leipz.,  1902,  xlviii,  163. 
Rubow:  Ueber  die  Lecithingehalt  des  Herzens  und  der  Nieren  unter  normalen  Verhalt- 

nissen,  Hungerzustande  und  bei  der  Fettigen  Degeneration,  Arch.  f.  exper.  Path.  u. 

Pharmakol,  Leipz.,  1904-5,  Hi,  173! 
Welch,  W.  H.:  Cartwright  Lectures  on  the  Nature  of  Fever,  Medical  News,  N.  Y.,  1888. 
Hasenfeld,  A.,  and  Fenyvessy,  B.:  Ueber  die  leistungsfiihigkeit  des  fettig  entarteten  Her- 
zens, Berl.  klin.  Wchnschr.,  1899,  xxxvi,  80,  125,  150. 
De  la  Camp,  O.:  Quoted  on  page  145. 
Kraus,  F.:  Die  klinische  Bedeutung  der  fettigen  Degeneration  des  Herzmuskels  schwer 

anaemischer  Individuen,  Berl.  klin.  Wchnschr.,  1905,  xlii,  p.  44A. 


IX. 

AFFECTIONS  OF  THE  MYOCARDIUM. 

A  certain  amount  of  degeneration  in  the  fibres  of  the  heart  muscle 
occurs  during  the  course  of  every  acute  febrile  disease  or  intoxication.  As 
has  been  seen  in  previous  chapters,  the  heart  under  these  conditions  exhibits 
signs  of  overstrain,  and  the  diagnosis  of  myocarditis,  therefore,  depends 
upon  the  degree  rather  than  the  mere  existence  of  cardiac  weakness. 
However,  in  certain  cases  the  signs  of  cardiac  weakness  overshadow  those 
of  the  original  disease  and  it  is  in  these  that  acute  myocarditis  is  usually 
recognized.  The  chronic  changes,  however,  which  follow  long  after  the 
original  disease  has  subsided,  present  a  less  complicated  picture  and  there- 
fore are  more  easily  recognized. 

PATHOLOGICAL    ANATOMY. 

The  lesions  of  acute  and  chronic  myocarditis  are  merely  different 
stages  in  a  process  which  is  more  or  less  continuous.  The  lesions  of  chronic 
myocarditis  are  always  preceded  by  the  acute  lesions,  but  the  degeneration 
may  not  be  so  severe  at  any  of  the  earlier  periods  as  to  give  rise  to  symp- 
toms of  cardiac  weakness. 

In  the  first  stage  of  acute  myocarditis  there  is  injury  and  degeneration 
of  the  muscle-fibres,  with  oedema  about  them,  and  infiltration  of  polymorpho- 
nuclear or  mononuclear  cells  into  the  oedematous  spaces  between  the  fibres. 

Degenerative  Changes. — The  degenerative  changes  which  take 
place  in  the  heart  muscle  are:  (1)  parenchymatous  degeneration, 
(2)  fatty  degeneration,  (3)  hyaline  and  amyloid  degenera- 
tion, (4)  calcareous  degeneration,  and  (5)  fragmentation. 

Parenchymatous  degeneration  of  the  heart  muscle  was  first 
described  by  Virchow  and  Boettcher.  The  muscle-fibres  swell,  lose  their 
striation,  and  the  plasma  contains  numerous  granules  of  an  albuminous 
material,  probably  altered  muscle  proteid  (myosin).  They  retain  their 
contractile  power  to  a  certain  extent,  but  its  force  at  this  stage  is  somewhat 
impaired,  and  the  cell  may  subsequently  return  to  normal  without  under- 
going complete  necrosis.  In  the  more  severely  injured  cells  the  nucleus 
is  destroyed,  the  sarcoplasm  becomes  filled  with  vacuoles,  takes  on  a  basic 
stain,  and  is  gradually  absorbed,  leaving  only  the  sarcolemma.  Often,  but 
not  always,  parenchymatous  and  fatty  degeneration  go  on  in  the  same 
fibre,  the  fat  being  deposited  as  the  proteid  is  removed. 

In  some  cases  fibres  undergo  hyaline  or  waxy  degeneration 
(Zenker)  and  present  an  absolutely  homogeneous  appearance,  taking  up  the 
acid  stains  (protoplasmic)  with  great  avidity.  In  rarer  cases  there  is  a 
calcareous  degeneration  with  deposit  of  calcium  salts  in  the  muscle- 
cells.     These  cells  then  take  up  the  basic  (or  nuclear)  stains  (description  of 

224 


AFFECTIONS   OF   THE   MYOCARDIUM. 


225 


a  case  and  discussion  of  the  literature  is  to  be  found  in  the  article  of  E.  K. 
Cullen).  The  degeneration  is  never  uniformly  distributed  throughout  the 
cells,  not  all  the  cells  being  affected  at  once  or  in  the  same  degree. 

Occasionally  the  heart  muscle-cells  show  peculiar  splits  extending  transversely  across 
the  whole  or  part  of  the  cell.  This  condition  is  known  as  "fragmentation."  The 
fibres  may  show  no  other  signs  of  degeneration,  the  transverse  striations  may  be  clear,  and 
the  longitudinal  strise  may  be  distinct  up  to  the  line  of  the  fracture.  Fragmentation  has 
been  found  after  death  from  a  tremendous  variety  of  causes,  even  in  individuals  dying  from 
accident.  It  does  not  seem,  therefore,  to  be  a  sign  of  specific  degeneration.  Dietrich's 
attempts  to  prove  it  an  artefact,  and  either  to  exclude  it  when  once  present  or  to  bring  on 
fragmentation  by  allowing  the  heart  to  pass  through  various  stages  of  decomposition,  have 
been  unsuccessful,  and  Buhlig  in  a  very  careful  research  seems  to  have  shown  that  it 
is  an  artefact  which  is  produced  when  the  microtome  knife  cuts  at  right  angles  to  the 
muscle-fibres.  This  observation  still  requires  confirmation.  Otherwise  the  consensus  of 
opinion  seems  to  be  that  fragmentation  is  the  result  of  some  change  in  the  muscle-fibres 
occurring  during  the  death  agony,  and  that  it  is  not  to  be  regarded  as  a  degeneration. 

As  illustrating  the  frequency  of  the  several  types  of  myocardial  degeneration  Romberg 
finds  the  following  frequency  in  29  cases: 

Typhoid  fever — 11  cases:  Parenchymatous  (albuminous)  degeneration,  moderate  or 
intense  10:   fatty,  present  6,  absent  5;  hyaline  or  waxy  (slight)  2,  absent  9. 

Scarlet  fever — 10  cases:  Albuminous  degeneration,  present  8,  absent  1,  not  noted  1; 
fatty,  intense  1,  moderate  1,  absent  8;  hyaline  or  waxy,  moderate  3,  absent  7. 

Diphtheria — 8  cases:  Albuminous,  intense  1,  moderate  4,  absent  3;  fatty,  intense  5, 
absent  3;  hyaline  or  waxy,  present  2,  absent  6. 


Fig.  144. — Infiltration   along   the  course  of   the   blood-vessels  in  subacute  myocarditis.     Blood-vessels 
injected.     A.   Low  power.     B.  Same,  higher  power.      (Photomicrograph  by  Dr.  C.  S.  Bond.) 

Distribution  of  Myocardial  Changes. — In  man,  according  to  Krohl,* 
acute  myocardial  lesionsare  particularly  common  in  the 
papillary   muscles   of    the    left    ventricle    and    in    the    mus- 

'  Examination  of  Specimens. — In  cases  in  which  the  state  of  the  myocardium  is 
of  importance,  the  microscopic  structure  of  the  heart  muscle  should  always  be  examined 
by  the  method  of  Krehl.  Krehl  cuts  the  heart  into  cubical  blocks  1  cm.  in  size,  numbering 
them  in  order  so  that  the  exact  location  of  each  block  can  be  accurately  determined.  These 
blocks  are  fixed  in  Miiller's  solution  and  a  section  or  two  from  each  is  examined.  In  this 
way  a  very  thorough  idea  of  the  extended  distribution  of  lesions  may  be  gained,  and  a  study 
of  a  very  few  hearts  thus  reveals  more  accurate  knowledge  than  can  otherwise  be  gained 
from  a  large  number  of  organs  examined  less  thoroughly. 
15 


226 


DISEASES   OF  THE   HEART   AND    AORTA. 


culature  about  the  left  auriculoventricular  ring.  Pearce 
and  Fleisher  and  Loeb  have  produced  in  rabbits  myocardial  lesions  having 
the  same  distribution  by  the  injection  of  adrenalin  (Pearce)  or  adrenahn 
with  spartein  or  caffeine  (Fleisher  and  Loeb).  Roy  and  Adami  have 
shown  that  cedema  occurs  most  readily  in  these  regions  during  experi- 
mental cardiac  overstrain. 

In  contrast  to  the  lesions  upon  the  valves,  the  toxic  or  infective  agents 
giving  rise  to  lesions  of  the  myocardium  do  not  spread  through  the  walls 
from  the  cavity  of  the  ventricles,  but  are  carried  into  the  heart  muscle 
through  the  coronary  arteries  and  distributed  through  their  finer  branches. 

The  foci  of  inflammation  whether  of  bacterial 
or  toxic  origin  usually  arise  within  the  lymph 
spaces  around  the  arteries,  which  they 
surround  in  sleeve,  cuff,  or  signet- 
ring   distribution. 

Abscess.  —  The  form  which  the  foci  as- 
sume depends  chiefly  upon  the  nature  and 
properties  of  the  infective  agent.  If  the 
virulence  of  the  germ  is  great,  abscesses  may 
be  produced  in  the  heart  muscle  (suppurative 
myocarditis)  as  elsewhere  in  the  body.  These 
abscesses  are  usually  produced  by  small  septic 
thrombi  which  plug  the  minute  branches  of 
the  arteries.  Under  the  influence  of  the  fibrin 
ferment  secreted  by  the  bacteria,  the  vessel 
soon  becomes  completely  filled  with  a  throm- 
bus, an  area  of  ischsemia  results  in  the  heart 
muscle,  which  quickly  becomes  infected  and 
breaks  down  to  form  an  abscess.  These  ab- 
scesses vary  in  size  from  a  submiliary  nodule 
to  a  cavity  separating  the  muscle  layers  in  the 
entire  interventricular  septum.  They  are 
usually  produced  by  the  pyogenic  cocci  in 
septicaemia  or  following  trauma  to  the  heart  (see  page  519).  The  outcome 
is  usually  fatal.  Occasionally  there  is  rupture  of  the  ventricle  through 
the  necrotic  portions  of  the  wall. 

"Rheumatic"  Foci. — In  the  less  virulent  infections,  such  as  rheuma- 
tism, typhoid  fever,  influenza,  the  foci  do  not  undergo  suppuration,  but 
the  lymph  spaces  around  the  arteries  and  capillaries  are  filled  with  cellular 
infiltration,  polymorphonuclear  in  most  of  the  acute  infectious  diseases, 
while  mononuclear  cells  predominate  in  myocarditis  from  typhoid  fever 
and  subacute  rheumatism. 

Since  rheumatic  fever  is  perhaps  the  most  common  cause  of  myocar- 
ditis, the  lesions  which  it  produces  are  of  particular  interest.  Romberg,. 
Aschoff,  Geipel,  and  Coombs  have  called  attention  to  the  presence  of  small 
submiliary  foci  0.1-0.2  mm.  in  diameter,  which  occur  with  great  frequency 
in.  rheumatic  patients,  especially  in  the  musculature  about  the  mitral  ring. 
Each  focus  consists  of  a  hyaline  centre  formed  by  agglutinative  thrombosis 
within  a  capillary.    About  this  there  is  a  zone  of  giant  cells  each  containing 


Fig.  145. — Septic  myocarditis  with 
multiple  abscesses  in  the  heart  wall. 
The  arrows  point  to  the  abscesses. 


AFFECTIONS   OF   THE   MYOCARDIUM. 


227 


2-4  nuclei,  and  these  in  turn  are  surrounded  by  a  wider  zone  of  mononuclear 
cells  interspersed  with  eosinophiles.  The  writers  mentioned  regard  these 
foci  as  pathognomonic  of  rheumatism,  although  they  may  bear  only  the 
general  features  of  a  subacute  inflammation  about  an  area  of  hyahne  throm- 
bosis. Indeed  the  most  typical  specimen  of  these  found  in  the  Johns 
Hopkins  Pathological  Museum  was  seen  in  a  case  of  non-rheumatic  myocar- 
ditis. On  the  other  hand,  Freund  has  reported  a  case  of  acute  rheumatic 
myocarditis  in  which  the  infiltration  was  mainly  polymorphonuclear. 

Bracht  and  Wachter  have  recently  produced  arthritis,  endocardiiis,  and  myocarditis 
with  lymphocytic  infiltrations  in  animals  by  injection  of  cultures  of  diplococci  obtained 
from  two  cases  of  acute  articular  rheumatism.  These  infiltrations  contrast  sharply  with 
the  polymorphonuclear  infiltrations  usually  produced  by  pyogenic  streptococci. 


Fig.  146. — Photomicrograph  showing  an  abscess  in  the  heart  muscle.  A.Lowpower.  B.  Same,  higher  power. 

Subsidence  of  Lesions. — The  changes  which  occur  in  the  myocardium 
when  the  patient  recovers  from  the  acute  infection  or  intoxication,  which 
is  the  causal  factor,  vary  both  with  duration  and  intensity  of  the  disease 
and  the  rapidity  and  completeness  of  the  recovery.  If  the  causal  factor 
completely  disappears  and  its  sojourn  in  the  body  has  been  a  short  one,  no 
permanent  changes  may  have  taken  place.  The  oedema  of  the  fibres  disap- 
pears, the  cellular  exudate  may  be  absorbed  in  toto,  and  the  myocardium 
may  resume  its  normal  appearance.  If  areas  of  fibres  have  been  destroyed 
their  place  may  be  taken  by  scar  tissue.  But  if  the  duration  of  the  process 
has  been  so  long  that  connective  tissue  has  begun  to  be  formed  in  the 
exudate,  the  traces  are  no  longer  obliterated  and  a  chronic  myocarditis 
has  set  in. 


PATHOLOGICAL    PHYSIOLOGY. 

As  has  been  seen  in  previous  chapters,  hearts  whose  muscle 
is  injured  become  dilated  upon  comparatively  slight 
exertion,  while  healthy  hearts  resist  dilatation  in  spite  of  tremendous 


228  DISEASES   OF   THE   HEART   AND    AORTA. 

exertion.  Moritz  and  Dietlen,  whose  X-ray  studies  have  demonstrated 
that  the  normal  heart  becomes  smaller  in  severe  exercise,  have  shown  that, 
on  the  contrary,  the  heart  whose  muscle  is  diseased  undergoes  tremendous 
dilatation.  Nevertheless  it  may  maintain  a  normal  or  even  heightened 
blood-pressure  without  apparent  effort,  and  except  for  the  dilatation  may 
present  no  other  signs  of  abnormality.  It  is  more  common  in  conditions 
of  acute  myocardial  change  to  have  a  low  blood-pressure,  but  this  is  due 
to  the  fact  that  the  toxic  substances  which  injure  the  heart  muscle  also 
depress  the  vasomotor  centre.  The  low  blood-pressure  is  due  to  the  latter 
influence  and  not  to  the  weakness  of  the  heart. 

These  facts  were  brought  out  by  very  interesting  studies  of  the  physiology  of  the 
heart  muscle  after  injections  of  diphtheria  toxin  which  were  made  by  Roily  and  later  by 
V.  Stejskal.  Roily  used  a  dose  of  toxin  which  just  killed  his  rabbits  in  twenty-four  hours, 
and  then  began  his  experiments  about  twenty-two  hours  after  the  injection.  He  found 
that  at  this  time  the  blood- pressure  antl  pulse-rate  of  the  animal 
were  still  quite  normal,  and  that  the  heart  was  still  able  to  respond  well  to 
increased  work  thrown  upon  it  by  compressing  the  abdominal  aorta,  etc.,  and  that  the  blood- 
pressure  increased  considerably.  About  half  an  hour  before  death,  however,  the  blood- 
pressure  began  to  fall,  owing  to  loss  of  vasomotor  tone,  as  had  been  shown  by  Romberg. 
Even  at  this  time  the  heart  was  still  strong  enough  to  respond  by  a  second  rise  of  blood- 
pressure  upon  clamping  the  abdominal  aorta.  Very  .soon  after  this,  however,  within  a 
few  minutes,  the  rate  became  irregular  and  the  heart  weak- 
ened completely.  V.  Stejskal's  results  were  similar.  The  action  of  the  diphtheria 
toxin  had  not  been  immediate,  but  it  had  required  several  hours  to  combine  with  the  heart 
muscle,  after  which  its  weakness  was  manifest. 

The  conclusion  reached  by  Roily  and  v.  Stejskal  is  that  the  heart 
remains  competent  in  spite  of  muscular  weakness  until 
a  certain  degree  of  strain  is  imposed  upon  it,  when  it 
suddenly  crosses  the  threshold  that  leads  to  failure,  dilatation,  and  even 
death.  The  threshold  of  cardiac  overstrain  in  the  healthy  heart  is  at  a 
much  higher  level. 

Arrhythmia  in  Acute  Myocarditis. — Irregularity  of  the  pulse  cannot  be 
brought  about  by  injuring  the  myocardium  by  injection  of  alcohol,  iodine, 
or  even  KCN,  but  often  occurs  in  man  as  a  result  of  myocardial  lesions, 
especially  after  exercise  and  overstrain.  Gerhardt,  Miiller,  and  Schonberg 
have  called  attention  to  the  association  of  irregularity  with  structural 
changes  and  paralyses  of  the  right  auricle.  In  mitral  disease  it  is  probable 
that  irregularity  arises  in  the  left  auricle  rather  than  in  the  right,  since  the 
latter  is  then  not  the  seat  of  pathological  conditions.' 

Bradycardia  is  met  with  in  the  late  forms  of  diphtheric,  influenzal, 
and  pneumonic  myocarditis  and  occasionally  during  the  febrile  stage.  It 
is  often  vagal  in  origin,  but  is  sometimes  due  to  depressed  conductivity 
of  the  auriculoventricular  bundle,  the  ventricle  responding  only  to  alter- 
nate contractions  of  the  auricle  (2  :  1  rhythm).  It  is  probable  that  under 
these  conditions  toxic  myocardial  changes  have  taken  place  in  the  bun- 
dle (Mackenzie).  It  is  not  unlikely  that  some  of  the  sudden  deaths 
during  convalescence  from  diphtheria  may  be  due  to  this  cause  (Dunn, 
see  page  478). 

'  More  fully  discussed  in  chapter  on  Mitral  Stenosis. 


AFFECTIONS   OF   THE   MYOCARDIUM.  229 


SIGNS    AND    SYMPTOMS. 

The  most  characteristic  sign  of  myocardial  weak- 
ness is  dilatation  of  the  heart  (see  page  227) .  The  heart 
is  usually,  but  by  no  means  always,  rapid,  the  sounds  may  be  clear  but  are 
usually  short  and  sharp;  they  may  be  embryocardiac  in  rapid  hearts;  a 
gallop  rhythm,  especially  of  the  presystolic  type,  may  be  present, 
or  the  sounds  may  be  definitely  split  (reduplicated).  It  is  also  very  com- 
mon to  hear  soft  systolic  murmurs  over  the  apex  or  the  tri- 
cuspid area,  due  to  functional  insufficiencies  at  the  auriculoventricular 
orifices  (see  page  140),  or  to  hear  the  "accidental"  systolic  murmur  in 
the  pulmonary  area.  The  second  pulmonic  sound  is  usually  ac- 
centuated  from  stasis  in  the  pulmonary  vessels. 

Clinically,  uncomplicated  myocarditis  is  met  with  in  the  course  of  the 
febrile  diseases  and  the  intoxications,  especially  alcohol- 
ism, phosphorus  poisoning,  and  ptomaine  poisoning.  It  is  present 
also  in  a  certain  degree  in  almost  every  case  of  acute  endocarditis  or  peri- 
carditis, where  it  is  but  part  of  the  general  "carditis." 

Its  manifestations  are  simply  those  of  acute  heart  failure  or  of  cardiac 
overstrain  occurring  while  at  rest  or  upon  very  slight  exertion.  The  symp- 
toms are,  therefore,  sometimes  those  of  broken  pulmonary 
compensation  (failure  of  the  left  ventricle,  page  139),  sometimes 
those  of  broken  systemic  compensation  (failure  of  the 
right  ventricle) ,  according  as  the  left  ventricle  or  the  right  is  the  one  most 
affected.  In  many  cases  there  are  attacks  of  precordial  pain 
amounting  almost  to  angina  pectoris,  coming  on  when  the  heart  is  acutely 
dilated  after  excitement  or  exertion. 

ACUTE    MYOCARDITIS    IN    RHEUMATIC    FEVER. 

Although  weakening  of  the  heart  is  one  of  the  most  important  factors 
in  general  asthenia  that  accompanies  or  follows  tonsillitis  or  rheumatic 
fever,  it  does  not  often  kill  the  patient  and  hence  is  not  often  a  striking  fea- 
ture at  the  autopsy  table. 

The  following  history  illustrates  the  course  in  fatal  cases,  showing  (1) 
the  gradual  insidious  onset,  (2)  shortness  of  breath,  extreme  weakness, 
and  finally  ascending  OBdema,  (3)  dilatation  of  the  heart,  with  oedema  and 
degenerative  changes  in  the  heart  muscle,  without  either  hypertrophy, 
fibrous  changes,  or  valvular  lesion. 

Case  of  Acute  Rheumatic  Myocarditis. 

Annie  Jones,  female,  colored,  48,  admitted  July  5,  1904,  complaining  of  "  rheu- 
matism,'' of  which  she  has  had  attacks  for  many  years,  especially  marked  during  the 
last  two  years.  The  knees  and  shoulders  have  been  the  joints  most  frequently 
affected.  She  has  had  no  other  infectious  diseases  and  the  previous  history  is  otherwise 
negative.  No  shortness  of  breath  nor  palpitation.  During  past  four  weeks  has  been  com- 
pelled to  sleep  upright  in  a  Morris  chair,  and  has  had  incontinence  of  fiEces. 

Physical  Ex,\mination. — -Patient  is  a  very  stout  colored  woman,  lying  quietly 
on  her  back  in  bed.     Pupils  equal  and  react  to  light  and  accommodation.    Chest  clear. 

Heart. — Impulse  is  not  visible.  Relative  cardiac  dulness  extends  13 
cm.    to  left  of  midline  in  fourth  interspace,  30  cm.  to  the  right.     First  sound  at  apex 


230 


DISEASES   OF   THE   HEART   AND    AORTA. 


is  very  loud  and  not  .perfectly  clear,  though  there  is  no  definite  murmur.  Second  sound 
resembles  the  first  in  quality  but  is  clear.  Pulse  regular,  of  good  volume,  rather  high 
tension,  100  per  minute.    Vessel  wall  somewhat  thickened. 

Abdomen  is  extremely  large  and  swollen;  there  is  dulness  in  dependent  portion. 
Liver  is  not  enlarged.  Legs  are  extremely  swollen  and  indurated;  do  not  even  pit  on 
pressure.  Knee-  and  ankle-joints  much  swollen  and  stiff.  A  round  perforating  ulcer  is 
present  at  left  heel.    No  disturbance  of  sensation  anywhere. 

Temperature  99°;  red  blood-corpuscles  4,046,000;  haemoglobin  55  per  cent.;  leuco- 
cytes 3800. 

Ordered  rest  in  bed;  soft  diet;  diuretin  1  Gm.  (gr.  xv)  q.  4  h.;  ulcer  of  foot  to  be 
irrigated  with  sol.  potass,  permang.  1:20000  b.  d.  On  July  7,  ordered  tinctura  dig- 
italis 1  c.c.  (T(\,xv)  q.  4  h.,  ad  dos.  viii;  this  was  then  repeated  and  continued  throughout 
the  course  of  disease.  Spts.  glycerylis  nitrat.  gtt.  ii,  q.  4  h.,  alternating  with  sod.  nitrit. 
0.3  Gm.  (gr.  v)  q.  4  h.;  morphin.  sulph.  0.008  Gm.  (^  gr.)  p.r.n. 

July  12.  Heart's  action  irregular;  first  sound  reduplicated  over  tricuspid  area;  no 
murmurs.  July  15.  There  is  a  large  perforating  ulcer  just  below  coccyx.  This  was  irri- 
gated with  potass,  permanganate  1  :  20000  and  packed  with  iodoform  gauze.  July  16. 
Temperature  106°;  percussion  note  impaired  at  left  base  behind,  where  breath  sounds  are 
absent.  A  few  rales  have  previously  been  heard  in  this  area.  Ordered  strychnine  sulph. 
0.003  Gm.  (jVgr.)  and  digitalin  0.003  Gm.  (iV  gr.)  hypo.  q.  4  h.  At  7.30  p.m.,  respiration 
shallow  with  expiratory  grunt.    At  11.00  became  unconscious,  and  died  at  12.45. 

Autopsy  showed  about  1  litre  of  fluid  in  peritoneal  cavity;  congestion  of  lower  lobe 
of  lungs. 

Heart . — Several  opaque  white  patches  over  epicardium,  one  with  a  diameter  of 
3  cm.  Coronary  arteries  soft  and  smooth.  Heart  muscle  soft,  flabby, 
and  of  yellowish -brown  color,  studded  with  numerous  small 
opaque   white  areas.     The  muscle  bundles  are  widely  separated  nuclei.    Lender  the 

microscope  the  muscle-fibres  are  seen  to  be 
swollen  ;  little  new  growth  of  interstitial  connective 
tissue.  Heart  weighs  250  Gm.  Slight  sclerosis  about 
base  of  aorta,  none  elsewhere.  Kidneys  normal  in  size, 
pale  and  cloudy.    Liver  shows  some  fatty  degeneration. 

DIPHTHERIC    AND    INFLUENZAL    MYOCARDITIS. 

Acute  myocarditis  is  the  chief  cause  of  death 
in  diphtheria  and  influenza.  In  these  conditions 
it  may  manifest  itself  either,  (1)  as  an  early  form 
during  the  course  of  the  fever,  or  (2)  as  a  late  form 
which  becomes  manifest  after  the  temperature 
has  fallen.  The  cases  of  diphtheric  myocarditis 
have  been  most  carefully  studied  by  Hibbard 
in  800  cases  with  119  deaths  (15  per  cent.)  at 
the  Boston  City  Hospital.  In  spite  of  the  high 
average  mortality,  the  mortality  was  less  than 
5  per  cent,  in  those  cases  in  which  the  pulse- 
rate  was  below  130  per  minute,  increasing  as  the  pulse-rate  increased 
above  that  figure.  Death  was  especially  frequent  in  those  cases  in  which 
a  gallop  rhythm  was  noted.  Bradycardia  (under  60  per  minute)  was  not 
a  severe  sign  in  adults  (14  cases  without  a  death;  only  2  with  cardiac 
symptoms),  whereas  in  cases  under  7  years  it  was  a  very  grave  sign 
(6  cases,  5  deaths).  In  all  Hibbard's  fatal  cases  there  were  both  acute 
myocardial  change  and  degeneration  of  the  fibres  of  the  vagus. 

Sudden  death  is  not  uncommon  in  cases  of  diphtheric  myocar- 
ditis; in  Dunn's  case,  from  the  onset,  heart-block  (Adams-Stokes  syndrome) 


Fig.  147. — Orthodiagraphic  out- 
lines of  the  heart  of  a  child  during 
the  course  of  a  severe  diphtheria. 
(After  Dietlen,  Munchen  med. 
Wchnschr.,  1905,  lii.)  +  +  +  ++, 
outline  on  fifth  day  (MR.  =  3.0 
cm.,  ML.  =  6.0  cm.,  L.  =  9.1  cm.); 

,  outline   on    seventh  day 

(MR.  =  3.5  cm.,  ML.  =  8.1  cm.,  L. 

=  12.4    cm.);    ,    outline    on 

twenty-sixth  day  (MR.  =  2.0  cm., 
ML.  =  6.5  cm.,  L.  =  9.3  cm.). 


AFFECTIONS   OF   THE   MYOCARDIUM.  231 

was  the  result  of  myocardial  change  in  the  vicinity  of  the  auriculoventricular 
bundle.  The  slow  pulse  also  is  often  due  to  partial  heart-block,  2  :  1 
rhythm,  though  this  may  be  due  to  overstimulation  of  the  vagus  as  well 
as  to  injury  of  the  bundle. 

Just  as  diphtheria  affects  the  myocardium  in  the  very  young,  influenza 
affects  it  in  the  aged.  Indeed  myocarditis  constitutes  one  of  the  gravest 
effects  of  this  disease,  and  is  especially  to  be  feared  after  the  sixth  decade. 

The  following  case  serves  as  an  example : 

Case  of  Influenzal  Myocarditis. 

Patient,  aged  75,  of  sedentary  habits,  rather  stout,  but  free  from  all  cardiac  symp- 
toms. Pulse  had  always  been  of  good  volume  and  regular.  Had  a  severe  attack  of 
influenza  in  March,  1903,  confining  her  to  bed  for  a  month.  No  special  car- 
diac features.  After  a  short  convalescence  she  was  again  able  to  be  up  and  about.  A  few 
days  later,  just  after  retiring,  she  had  a  severe  attack  of  cardiac  asthma, 
breathlessness,  orthopnoea,  and  slight  precordial  pain.  No  true 
angina.  Moderate  degree  of  cyanosis.  Pulse  small,  rapid,  irregular.  Cardiac  dulness 
slightly  enlarged.  Soft  systolic  murmur  heard  over  the  entire  heart.  The  attack  lasted 
half  an  hour,  symptoms  being  much  relieved  by  inhalations  of  amyl  nitrite. 

Patient  was  given  complete  rest  in  bed  for  a  few  days,  with  fluidextract  of  digitalis 
TT\,v  (0.3  c.c.)  three  times  a  day  and  soft  diet,  and  was  then  kept  at  rest  in  a  large  arm-chair. 
Gradual  convalescence.  Soon  became  free  from  symptoms,  but  pulse  remained  70  and 
irregular  and  she  was  compelled  to  refrain  from  every  effort  except  one  daily  trip  up  and 
down  stairs,  during  which  she  rested  at  each  step  long  enough  to  count  twenty.  In  June 
and  July,  1904,  she  had  several  similar  attacks,  and  though  she  improved  somewhat  her 
pulse  remained  permanently  irregular.  Died  suddenly  a  year  and  a  half  later,  death  fol- 
lowing six  weeks  after  a  severe  cellulitis  of  the  leg. 

Case  of  Subacute  Alcoholic  Myocarditis. 

B.  C.  S.,  reporter,  married,  aged  36,  admitted  to  the  service  of  Prof.  J.  O.  Hirsch- 
felder.  City  and  County  Hospital  of  San  Francisco,  January  23,  1905,  complaining  of 
shortness  of  breath  and  swelling  of  feet.  Father  and  brother  are  subject  to  rheumatism, 
and  patient  himself  had  swelling  of  joints  four  years  ago,  about  the  time  of  a  gonorrhcsal 
infection.  He  had  measles,  whooping-cough,  and  scarlet  fever  as  a  child,  and  typhoid 
fever  seven  years  ago.  Denies  syphilis.  Married,  but  has  had  no  children.  Uses  tobacco 
in  moderation,  but  drinks  whiskey  in  excess,  as  a  probable  result  of  which  he  has  fallen 
from  the  best  to  the  lowest  strata  of  society. 

Present  Illness. — Four  weeks  ago  while  in  the  midst  of  a  series  of  debauches  he 
noticed  that  his  shoes  became  tight,  and  in  a  few  days  his  legs  became  so  swollen 
that  he  could  not  put  on  his  drawers.  He  had  pain  in  the  legs  on  walking,  owing  to  the 
oedema.  He  also  felt  very  weak  and  became  exhausted  easily.  Has  had  shortness 
of  breath  on  exertion. 

Physical  Examination. — Well-nourished  man  of  good  color.  Tongue  and  uvula 
deviate  slightly  to  the  right.  General  glandular  enlargement.  Epitrochlears  palpable. 
Chest  negative  except  for  a  few  moist  rales  over  right  axilla  and  base. 

Heart . — Cardiac  impulse  not  visible.  Relative  cardiac  dulness  extends  to  12.5 
cm.  from  midline  in  fifth  interspace  (3  cm.  outside  mammillary  Hne),  4  cm.  to 
right  of  midline  and  above  to  the  third  rib.  Sounds  are  very  rapid,  the  first  sound  every- 
where replaced  by  a  systolic  murmur  which  is  loudest  at  the  apex;  not  transmitted  to  the 
axilla;  pulmonic  second  accentviated.  Pulse  108,  regular  in  force  and  rhythm,  low  tension, 
fairly  good  volume.    Radial  artery  not  palpable. 

Liver  just  palpable.  No  scar  on  genitalia.  Lower  extremities  are  covered 
with  pediculi  and  raw  scratch  marks.  Marked  oedema  of  both  legs.  Urine  nega- 
tive, sp.  gr.  1028. 

Ordered  liquid  diet;  fluidextract  digitalis  0.3  c.c.  O^v)  q.  4  h.;  spir.  glycerylis  nitratis 
1  gtt.  q.  4  h.;  sol.  magnes.  sulphat.  sat.  30  c.c.  (oi);   ung.  zinci  oxid.  to  legs. 


232  DISEASES   OF   THE   HEART    AND    AORTA. 

Jan.  30.  Pulse  slow  and  somewhat  irregular,  venous  tracing  show- 
ing that  some  of  the  auricular  impulses  did  not  reach  the  ventricle  (2  :  1  hearf-block). 
Given  atropine  0.0015  Gm.  (3  gr.)  at  12.45  p.m.  At  2  00  p.m.,  max.  pr.  135,  min.  75- 
80.  Pulse-pressure  60 X  pulse-rate  60  =  3600.  Pulse-rate  absolutely  regular,  as 
shown  in  the  brachial  artery  tracing  taken  at  1.45  p.m.  Digitalis  was  now 
discontinued. 

Feb.  2.  QCdemagone.  Soft  systolic  murmur  still  present  at  apex.  Pulse-rate  72,  abso- 
lutely regular,  responding  to  all  impulses  from  the  auricle.    It  never  again  became  irregular. 

Feb.  11.  Feels  quite  strong.  Up  and  about.  Heart  has  been  regular  and  all  mur- 
murs gone. 

March  2.  Has  had  slight  swelling  of  feet.  Was  again  put  to  bed.  The  swelling 
disappeared  within  24  hours. 

In  a  few  days  the  patient  was  again  up  and  about,  and  in  a  week  or  ten  days  later  was 
allowed  to  continue  his  work  in  the  pantry.  Was  discharged  apparently  cured  about 
May  15. 

DIAGNOSIS. 

As  has  been  seen,  the  diagnosis  of  acute  myocarditis  in  many  cases  is 
made  more  by  inference  than  by  definite  signs.  The  presence  of  symptoms 
of  cardiac  weakness  in  an  infectious  disease,  out  of  proportion  to  the 
severity  of  the  latter  or  to  the  apparent  severity  of  the  endocardial  lesion, 
is  presumptive  evidence  of  severe  myocardial  involvement.  The  symptom- 
complex  of  restlessness  or  marked  dulness,  constriction  over  the  chest,  and 
precordial  pain,  vomiting,  cyanosis,  and  increase  in  the  area  of  cardiac 
dulness,  during  or  after  an  attack  of  an  infectious  disease  or  of  delirium 
tremens,  is  practically  pathognomonic.  The  presence  of  a  systolic  murmur 
at  the  apex  and  over  the  body  of  the  heart,  which  may  even  be  transmitted 
to  the  axilla  but  which  disappears  during  convalescence,  added  to  the  other 
symptoms  above  mentioned,  would  indicate  myocarditis  rather  than  endo- 
carditis. It  must  be  borne  in  mind,  moreover,  that  the  presence  of  true 
endocarditis  or  pericarditis  is  evidence  in  favor  rather  than  against  the 
presence  of  an  additional  myocarditis,  and  that  in  the  acute  form  the  symp- 
toms are  quite  as  liable  to  be  due  to  the  insufficiency  of  the  muscle  as  to 
the  valves.  On  the  other  hand,  just  as  a  most  acute  nephritis  may  be  pres- 
ent without. the  presence  of  albumin  or  casts  in  the  urine,  so  acute  myo- 
cardial changes  may  be  present  without  definite  signs  of  cardiac  weakness 
other  than  a  tendency  to  fatigue.  In  view  of  the  observations  of  de  la 
Camp,  Moritz,  Dietlen,  and  Hornung,  myocardial  changes  may  be  diag- 
nosed in  cases  in  which  the  heart  undergoes  transitory  dilatation  (with 
or  without  transitory  valvular  insufficiencies)  upon  comparatively  slight 
exertion.  The  cardiac  area  under  such  conditions  must  be  most  carefully 
outlined,  if  possible  with  the  orthodiagraph.  In  the  absence  of  the  latter 
careful  percussion  may  often  suffice.  The  changes  must  be  1  cm.  or  more 
before  they  should  be  considered  as  definite. 

TRE.\TMENT. 

The  management  of  a  case  of  acute  myocarditis  differs  essentially  from 
that  of  the  chronic  form,  owing  to  the  fact  that  in  the  former  the  changes 
in  the  muscle  may  be  of  a  temporary  character,  while  in  the  latter  the 
changes  are  permanent.  Accordingly,  in  the  acute  form  the  aim 
is    to    allow   the    muscle   to   return   to   its   normal   state. 


AFFECTIONS   OF  THE   MYOCARDIUM.  233 

while  in  the  chronic  form  this  cannot  be  hoped  for, 
and  the  treatment  is  directed  toward  obtaining  the  best  functional  result 
possible  in  the  changed  muscle  that  is  left.  The  one  aims  at  bringing 
about  subsidence,  the  other  at  inducing  hypertrophy. 

Accordingly,  even  in  the  mildest  form  of  acute  myocarditis  rest  is  all- 
important — c  omplete  rest  in  bed  until  the  degenerative 
changes  in  the  muscle  have  subsided.  This  is  especially 
important,  since  cardiac  overstrain  sets  in  very  easily  in  such  hearts,  and 
it  is  probable  that  this,  in  even  the  slightest  degree,  increases  the  injury 
to  the  muscle-fibres  as  well  as  the  extent  of  the  interstitial  oedema  and 
infiltration.  The  patient  should  be  kept  in  bed  at  least  two  weeks  after 
any  indications  of  myocardial  weakness  have  subsided,  and  if  possible 
until  the  pulse-rate  has  again  become  slow.  An  easily  digestible  diet  equiva- 
lent to  about  1000-1500  calories  should  be  enforced  (see  page  167),  frequent 
feeding  of  small  quantities  being  resorted  to  in  the  place  of  three  compara- 
tively large  meals. 

An  ice-bag  should  frequently  be  applied  to  the  precordium,  since  it 
tends  to  slow  the  heart-rate.  Some  writers,  especially  Caton,  strongly 
favor  the  application  of  small  blisters  to  the  precordium  and  the  administra- 
tion of  small  doses  (0.3  Gm.  or  5  gr.)  of  potassium  iodide,  but  it  is  extremely 
doubtful  whether  this  has  any  effect  upon  the  course  of  the  disease. 

If  anffimia  arises,  iron  should  be  ordered  in  some  form,  usually  as 
Blaud's  pills, — ferri  carbonas  saccharatus  (0.25  Gm.,  4  gr.), — or  Vallet's 
mass  (same  as  Blaud's  pills  with  honey  instead  of  sugar  but  more  perma- 
nent), or  elixir  ferri,  quininaeet  strythninaj  phosphatum  (4  c.c,  1  fluidrachm). 
If  constipation  or  other  digestive  disturbances  result,  ha^matin  or  some 
other  "organic"  iron  preparation,  that  is,  where  the  iron  is  combined  with 
proteid.  The  patient's  bowels  should  be  kept  freely  moving  without  effort, 
best  by  means  of  Rochelle  salts,  sodium  phosphate,  Epsom  salts,  or  Seidlitz 
powders.  The  effervescent  citrate  of  magnesia  usually  causes  greater 
abdominal  distention  than  is  desirable,  owing  to  the  upward  displacement 
of  the  diaphragm. 

Hypersensibility  to  Digitalis.  —  The  usefulness  of  digitalis  in  acute 
myocarditis  is  a  debatable  question.  Digitalis  acts  as  a  spur  to  the  heart 
and  raises  the  strength  of  the  contraction  until  it  enables  the  fibres  to  draw- 
on  their  reserve  force  at  each  contraction,  but  it  does  not  raise  the  limit 
strength.  When  that  limit  is  already  approached  it  spurs  them  too  far, 
and  drives  them  to  overstrain  and  even  to  death. 

Whether,  in  any  individual  case,  digitalis  will  do  good  or  harm  will 
depend,  therefore,  upon  the  degree  to  which  degenerative  changes  have 
progressed  and  the  amount  of  reserve  force  that  is  left.  Thus,  in  the  case 
of  B.  C.  S.,  the  myocardial  degeneration  was  slight  and  the  beneficial  action 
of  digitalis  was  marked.  With  A.  J.,  however,  the  case  was  different. 
Degeneration  had  reached  too  advanced  a  stage  and  the  drug  was  useless, 
perhaps  even  harmful. 

Even  the  heart  of  B.  C.  S.,  however,  manifested  the  abnormal  suscepti- 
bility of  such  hearts  to  digitalis,  since  it  produced  partial  block  and  extra- 
systoles  with  doses  which  barely  sufficed  to  slow  the  heart  of  the  average 
patient. 


234 


DISEASES   OF   THE   HEART    AND    AORTA. 


Moreover,  in  acute  myocarditis  the  heart  is  hypersensitive  to  digitalis. 
For  example,  in  the  case  of  B.  C.  S.,  a  normal  dose  produced  an  abnormally 
intense  reaction  with  signs  of  the  first  stage  of  digitaUs  poisoning— partial 
heart-block  and  extrasystoles.  Fortunately  in  this  case  the  good  effects 
outweighed  the  bad,  but  it  belonged  to  the  group  of  cases  which  prove  con- 
clusively that  in  acute  myocarditis  digitalis  should  always  be  given  in 
smaller  doses  than  would  be  used  for  a  heart  with  a  valvular  lesion  which 
showed  the  same  degree  of  heart  failure. 

Strychnine. — As  regards  strychnine,  both  its  beneficial  and  its  harmful 
effects  are  less  marked  than  those  of  digitalis.  It  is  therefore  less  liable  to 
overstep  the  limit  of  tolerance.  In  ordinary  doses  it  tends  to  increase  the 
cardiac  tonicity,  as  well  as  to  stimulate  the  cardiac  nerves,  the  respiratory 
and  vasomotor  centres,  so  that  it  becomes  a  valuable  drug  in  such  conditions. 

CHRONIC   MYOCARDITIS. 


PATHOLOGICAL    ANATOMY. 

Pathologically  the  chronic  inflammatory  changes  in  the  myocardium 
may  be  divided  into  three  groups: 

1.  Cicatricial  patches  or  scars  arising  from  the  healing  of  isolated  areas  of  inflam- 
mation (abscess  or  focal  infiltrations)  or  from  the  organization  of  areas  of  infarction. 

2.  Thickening  of  the  septa  that  separate  the  muscle  strands  (interfascicular  myo- 
fibrosis, Dehio)  occurring  when  the  heart  muscle  hypertrophies. 

3.  Diffuse  degeneration  of   the  muscle-fibres  with  invasion  of  the  fibre  bundles  by 
strands  of   connective  tissue   {cardiosclerosis,   Huchard;    interstitial   myofibrosis,   Dehio). 


Fig.  148. — Specimen  showing  a  cardiac  aneurism 
covered  with  pericardial  adhesions. 


Fig.  149.  —  Chronic  myocarditis   Ccardiosclero-sis). 


Cardiac  Cicatrices.— The  areas  of  cardiac  cicatrices  are  quite  common 
in  coronary  sclerosis,  in  which  they  represent  the  site  of  healed  infarcts 
in  the  area  supplied  br  the  affected  artery.  The  fibrous  tissue  composing 
the  scar,  relatively  poor  in  elastic  fibres,  is  weaker  than  the  rest  of  the 
heart  wall,  presenting  the  condition  termed  by  Ziegler  myomalacia  cordis, 
and  it  may  bulge  out  to  form  an  aneurism  of  the  heart  (Fig.  148). 


AFFECTIONS   OF   THE   MYOCARDIUM. 


235 


Spontaneous  rupture  occurs  in  such  areas,  and  death  occurs  from  hemor- 
rhage into  the  pericardium,  though,  according  to  Hamilton,  this  is  not  as 
frequent  a  cause  of  spontaneous  rupture  as  is  fatty  degeneration. 

On  the  other  hand,  the  smaller  areas  of  cicatrization  may  represent 
complete  obliteration. 

Interfascicular  Connective-tissue  Proliferation.  —  Interfascicular  myo- 
fibrosis or  hyperplasia  of  the  septa  between  the  bundles  is  to  be  regarded 
as  a  concomitant  of  cardiac  hypertrophy,  and  represents  a  strengthening 
rather  than  a  weakening  of  the  heart. 


A 

^^..^  .^ 

'^/^.i-"'^-  ^-    -      ■    - 

c 

^ 

■mt 

Sit . '     •  f  ' 

k 

-»    ■  ":.,    .  -Vf     - 

Fig.  150. —  Specimens  showing  chronic  myocarditis.  (Photomicrographs  by  Dr.  Chas.  S.  Bond.) 
A.  Intrafascicular  myofibrosis,  penetrating  into  the  bundles  of  muscle-fibres.  Hypertrophy  of  some  fibres; 
•atrophy  of  others.  B.  Coarse  strands  of  connective  tissue  penetrating  between  the  bundles  of  muscle- 
fibres  (interfascicular  myofibrosis). 

Cardiosclerosis. — The  most  important  form  of  lesion  in  chronic  myo- 
carditis is  the  interstitial  myofibrosis  or  cardiosclerosis.  This 
form  is  met  with  in  senile  hearts  and  in  most  cases  of  chronic  heart  failure. 
According  to  Dehio,  it  occurs  onl)^  in  those  hearts  which  have  been  sub- 
jected to  long-continued  dilatation,  frequently  in  hearts  in  which  hyper- 
trophy has  preceded  the  dilatation.  The  heart  muscle  is  oedematous. 
The  fibres  are  found  in  all  stages  of  change — normal  fibres,  large  healthy 
hypertrophic  fibres,  large  vacuolated  degenerating  fibres,  and  small  ones 
in  the  various  stages  of  atrophy — in  a  single  microscopic  field.  Many  of 
them  are  undergoing  fatty  degeneration.  In  response  to  the  well-known 
biological  law  that  wherever  the  parenchyma  of  an  organ  is  gradually 
destroyed  hyperplasia  of  the  interstitial  tissue  takes  its  place  (Weigert, 
.Dehio),  fine  strands  of  connective  tissue  are  seen  everywhere  winding 
their  way  between  the  muscle-fibres  and  gradually  taking  their  places. 


RELATION  OF  SITE  OF  MYOCARDIAL  LESION  AND   DISTURBANCE  OF  FUNCTION. 

Lesions  in  the  Ventricles.  —  Attempts  have  been  made  by  numerous 
investigators  to  demonstrate  a  definite  connection  between  the  exact  site 
of  the  myocardial  lesions  and  the  disturbance  of  function  met  with. 
Krehl,  who  under  Ludwig's  inspiration  was  the  pioneer  in  this  field,  inau- 


236 


DISEASES   OF  THE   HEART   AND    AORTA. 


gurated  the  method  of  studying  sections  from  every  part  of  the  heart,  and 
found  that  the  papillary  muscles  and  the  musculature  about  the  mitral 
ring  were  affected  with  great  frequency;  but  he  was  unable  to  establish  more 
definite  relations.  Albrecht's  attempt  to  do  this  for  the  various  muscle 
layers  discovered  by  Krehl  and  J.  B.  MacCallum  has 
called  forth  a  vigorous  contradiction  from  Aschoff 
and  Tawara,  who  have  made  a  most  careful  stud}'' 
of  150  pathological  hearts  by  Krehl's  method. 

On  the  other  hand,  His,  Erlanger,  Stengel, 
Schmoll,  and  a  host  of  others  have  demonstrated  that 
lesions  in  the  auriculoventricular  bundle  give  rise  to 
heart-block,  while  Aschoff,  Tawara,  Saigo,  Barker, 
and  Hirschfelder  have  shown  that  lesions  affecting 
one  branch  of  this  bundle  do  not  affect  the  contrac- 
tion of  either  ventricle.  Very  recently,  however,  H.  E. 
Hering  has  revived  interest  in  these  questions  by 
showing  upon  the  excised  heart  that  if  the  strand  of 
Purkinje  fibres  (conduction  system)  to  one  papillary 
muscle  is  cut  or  injured,  that  papillary  ceases  to  con- 
tract, although  the  rest  of  the  heart  continues  to  do  so. 
Lesions  in  the  Auricles. —  Studies  of  lesions  in 
the  auricles,  though  fewer,  have  been  still  more 
remunerative.  Dehio  and  his  pupil,  Radasewsky, 
demonstrated  that  in  chronically  dilated  hearts  the 
myocardial  changes  in  the  auricles  were  much  more 
marked  than  those  in  the  ventricles;  and  Schonberg, 
under  D.  Gerhardt's  direction,  has  shown  that  per- 
manent arrhythmia  with  auricular  paralysis  is  asso- 
ciated with  infiltrations  of  the  intervenous  area  which  correspond  to  the 
embryonic  sinus,  the  spot  at  which  the  cardiac  impulse  probably  originates. 


Fig.  151. — Hypertrophy 
of  some  muscle  bundles  in 
the  auricle  with  atrophy 
(transparency)  of  other 
areas.  (From  a  specimen 
in  the  Army  Medical  Mu- 
seum, Washington,  D.  C.) 


P.\THOLOGICAL    PHYSIOLOGY. 

The  chief  physiological  features  of  chronic  myocarditis  are: 

(1)  Oironic  weakness  of  the  heart,  with  tendency  to  undergo  dilatation  and  overstrain. 

(2)  Frequency  of  extrasystoHc  or  absolute  irregularities. 

Compensation  in  Myocarditis. — The  course  and  characteristics  of  myo- 
cardial weakness  have  been  fully  discussed  under  the  pathological  physiol- 
ogy of  cardiac  overstrain  (page  134).  Indeed,  the  persistence  of  a  primary 
overstrain  with  the  concomitant  oedema  of  the  heart  muscle  may  be  an 
important  factor  in  instituting  chronic  myocardial  changes  or  in  rendering 
the  heart  especially  susceptible  to  alcohol,  toxins,  tobacco,  or  other  influ- 
ences that  would  otherwise  not  affect  it.  The  changes  in  the  myocardium, 
the  lowered  tonicity,  the  persistent  oedema,  the  reduction  in  the  number 
of  efficiently  contracting  muscle-fibres,  all  tend  to  lower  the  threshold  of 
exertion  at  which  overstrain  is  ushered  in.  Whether  the  overstrain  mani- 
fests itself  as  a  broken  pulmonary  or  a  broken  systemic  compensation,  or 
as  both  together,  depends  upon  the  relative  and  absolute  strength  of  the 
two  ventricles  as  well  as  the  nature  of  the  exertion. 


AFFECTIONS   OF   THE   MYOCARDIUM. 


237 


BIood=pressure. — The  occurrence  of  such  overstrain  is,  however,  quite 
consistent  with  the  maintenance  of  a  normal  or,  especially,  a  high  blood- 
pressure.  This  high  blood-pressure,  strange  to  say,  is  in  itself  the  result 
of  the  chronic  cardiac  insufficiency  and  the  slowing  of  the  circulation.  With 
the  slowing  of  the  circulation  there  comes  asphyxia  of  the  med- 
ullary centres,  which  stimulates  them  and  brings  on  an  intense 
vasoconstriction.  The  vasoconstriction  narrows  the  arterial  bed  so  much 
the  arterial  pressure  must  be  raised  until  the  blood  flows  through  the  medul- 
lary centres  at  the  proper  rate.  The  weakened  heart  must  thus  rise  to  the 
occasion  and  sacrifice  itself  to  save  the  medullary  centres.  The  more  it 
fails  the  more  work  these  inexorable  centres  demand  from  it,  the  more 
they  throttle  the  arteries  in  their  struggle  to  get  blood  from  the  flagging 
heart.  The  more  the  arteries  are  throttled  the  greater  the  constriction, 
the  smaller  the  arterial  bed,  and  the  less  the  systolic  output  necessary  to 
overfill  the  arteries,  the  greater  the  force  necessary  to  drive  it.  The  heart 
may  therefore  empty  itself  incompletely  but  at  high  pressure  against  this 
high  peripheral  resistance,  while  the  increase  in  residual  blood  within  the 
ventricles  leads  to  dilatation  and  stasis.  This  condition  of  stasis  with  high 
pressure,  both  resulting  from  chronic  cardiac  weakness,  is 
usually  termed  "high  pressure  stasis''  (Hochdruckstauung) . 
Its  factors  actually  constitute  a  vicious  circle: 

Cardiac  weakening 

Increased  cardiac  effort  Slowed  circulation 

High  blood-pressure  through  medulla 

^  .     J 

Vasoconstriction 


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Fig.  152. —  Curve  of  blood-pressure  in  a  case  of  chronic  myocarditis,  showing  the  high  blood-pressure  per- 
sisting until  shortly  before  death.     (High-pressure  stasis.) 


This  accounts  for  the  fact  thaf  under  such  circumstances  venesec- 
tion may  raise,  digitalis  may  lower  the  blood-pressure,  and, 
on  the  other  hand,  the  blood-pressure  may  rise  rather  than  fall  as  death 
approaches  (Fig.  152). 

Arrhythmia.'  —  In  many  cases  of  chronic  myocarditis  the  heart  is 
irregular  in  both  force  and  rhythm,  especially  in  the  later  stages. 


238  DISEASES   OF   THE   HEART   AND   AORTA. 

The  chief  types  of  arrhythmia  observed  are : 

(1)  Extrasystoles    of    auricular    or    more    frequently    of    ventricular 

origin. 

(2)  Perpetual  absolute  arrhythm.ia. 

The  extrasystoles  seem  to  result  from  the  overloading  of  the 
chambers  in  which  they  arise;  the  perpetual  arrhythmia  both 
from  the  overloading  of  the  auricle  and  the  presence  of  chronic  myocardial 
changes  in  the  muscle  strands  of  the  intervenous  area  (embryonic  sinus 
reuniens).  (The  mechanism  and  significance  and  diagnosis  of  these  ar- 
rhythmias have  been  discussed  on  page  75.)  This  irregularity  in  itself 
also  exerts  an  unfavorable  action  upon  the  circulation.  When  the  site  at 
which  the  impulse  arises  is  diseased,  it  may  be  impossible  for  this  area  to 
generate  cardiac  impulses  in  rapid  succession,  and  hence  the  pulse  and  the 
circulation  may  remain  slow  in  spite  of  the  needs  of  the  body  for  increased 
aeration. 

SYMPTOMS    AND    SIGNS. 

From  the  above  cited  cases  it  will  be  seen  that  the  symptoms  of  chronic 
myocarditis  are  usually  those  of  gradually  developing  cardiac  weakness, 
progressively  increasing  weakness  and  dyspnoea,  at  first  on  exertion,  later 
when  at  rest,  and  finally  reaching  the  stage  of  orthopnoea.  Palpitation  is 
a  frequent  symptom;  sometimes  there  is  precordial  pain,  usually  behind 
the  sternum,  associated  with  sudden  dilatation  of  the  heart.  Swelling  of 
the  abdomen  and  often  pain  in  the  right  hypochondrium  are  associated 
with  the  stretching  of  the  capsule  of  the  liver  as  the  latter  enlarges. 
(Edema  ascending  from  the  feet  and  legs,  diminution  in  the  amount  of 
urine,  at  first  during  the  day,  with  frequent  and  increased  micturition  at 
night,  and  later  marked  diminution  in  total  urine  secretion  mark  the  later 
stages  of  broken  systemic  compensation. 

Physical  signs  are :  cyanosis;  dilatation  of  the  venules,  especially 
over  the  face;  general  engorgement  of  the  larger  veins,  often 
with  disappearance  of  the  "double"  venous  pulse,  and  either  total  absence 
of  the  pulsation  in  the  jugular  veins  or  appearance  of  a  "single"  venous 
pulse ;  often  irregularity  of  the  arterial  pulse,  usually  with  presence  of  marked 
arteriosclerosis;  increase  in  area  of  cardiac  dulness  to  right  or  felt;  occasion- 
ally a  catarrhal  jaundice  is  a  marked  sign  of  the  hepatic  engorgement. 

The  blood  count  often  shows  polycythaemia  and  high  hajmoglobin, 
without  change  in  leucocytes.  Blood-pressure  may  or  may  not  be  elevated ; 
but  in  most  cases  it  is  not  decreased.  Pulse  tracings  from  the  radial  and 
carotid  arteries  and  jugular  veins  often  show  persistent  absolute  arrhyth- 
mia, with  paralysis  of  the  auricles,  with  absence  of  signs  of  organic  valvular 
lesion.  There  may  be  a  more  or  less  transitory  soft  systolic  murmur 
present  at  apex  due  to  functional  mitral  insufficiency,  but  this  is  rarely 
transmitted  to  the  axilla  and  often  passes  off  during  treatment.  The  same 
applies  to  the  systolic  murmur,  which  may  be  loudest  over  the  tricuspid 
area.  There  is  usually  absence  of  diastolic  murmurs  except  in  cases  in 
which  functional  pulmonary  or  aortic  insufficiencies  are  suspected. 

A  mild  bronchitis  with  rales  and  some  oedema  is  common,  espe- 
cially at  right  base.     Enlargement  cf  the  liver,  with  either  systolic  impulse 


AFFECTIONS   OF   THE   MYOCARDIUM.  239 

(tricuspid  insufficiency)  or  systolic  retraction  (tumultuous  action  of  the 
right  ventricle),  occurs  in  the  later  stages. 

The  urinary  findings,  cardiac  symptoms,  and  clinical  course  in  such 
cases  may  be  very  similar  to  those  of  cases  which  are  primarily  renal  in  origin. 

Case  of  Chronic  Myocarditis. 

George  G.,  a  laborer,  aged  56,  was  admitted  to  Prof.  J.  O.  Hirschfelder's  wards  of 
the  City  and  County  Hospital,  San  Francisco,  on  April  21,  1905,  complaining  of 
asthma.  His  father  had  died  of  dropsy.  The  patient  had  had  rheumatism  in  18S7 
and  1895,  and  has  had  to  pass  water  during  the  night  for  some  years. 

Except  for  occasional  shortness  of  breath  he  was  well  until  two  weeks  before  admis- 
sion. H3  has  had  shortness  of  breath  for  the  past  two  years;  weakness  and  oedema  of  the 
feet  for  the  past  two  weeks. 

Physical  Examination.  —  Patient  is  a  fairly  nourished  man  ;  face  flushed  and 
venules  dilated.  No  marked  respiratory  distress.  Head  is  of  peculiar  shape.  Pupils  equal 
and  react  to  light  and  accommodation.  No  jaundice.  Definite  congenital  external  stra- 
bismus of  right  eye.  Eyes  move  well  in  all  directions.  Tongue  coated.  Throat  clear; 
tonsils  not  enlarged;  no  tracheal  tug.  No  enlargement  of  lymph-glands.  Thorax 
barrel-shaped.  Vocal  fremitus  equal  except  below  level  of  tenth  dorsal  vertebra  on  right 
side,  where  it  is  increased.  Percussion  note  everywhere  clear  except  over  this  area,  where 
breath  sounds  are  distant  and  a  few  rales  are  heard.  A  few  moist  rales  are  also  heard  over 
the  apices.  Heart . — Diffuse  but  feeble  impulses  in  sixth  left  interspace  15 
cm.  from  midline,  from  which  point  cardiac  dulness  extends  above  to  the  upper 
border  of  the  third  rib  and  6  cm.  to  the  right  of  the  midline  in  the  fourth  interspace.  Heart 
sounds  feeble  and  accompanied  by  a  soft  systolic  murmur.  Neither  sound 
at  base  specially  accentuated.  Pulse  very  feeble,  rapid,  and  irregular.  There  is  no  auricu- 
lar wave  upon  the  tracing  of  the  venous  pulse,  and  the  arrhythmia  is  devoid  of  any 
regularity  in  sequence.     Radial  arteries  are  very  sclerotic.     No  cEdema  of  feet  or  legs. 

Patient  has  some  cough,  raising  mucopurulent  sputum,  with  large  numbers  of  strepto- 
cocci but  no  influenza  or  tubercle  bacilli.  Urine  negative;  sp.  gr.  1010;  no  albumen, 
casts,  or  sugar. 

Ordered:  Soft  diet.  Pil.  cathart.  co.,  ii,  q.  n.;  sol.  magnesii  sulphatis  sat.,  30  c.c. 
(^i)  q.  A.M.;  fluidextract  digitalis,  0.3  c.c.  ("Iv)  q.  4  h.;  spir.  glycerylis  nitratis,  q.  ^  h., 
commencing  with  1  gtt.  and  increasing  1  gtt.  at  each  third  dose  until  patient  feels  throb- 
bing of  the  head  or  flushing  of  face,  after  which  next  dose  is  to  be  omitted,  and  subsequent 
doses  of  1  gtt.  less  than  the  last  are  to  be  then  given.  Morphin.  sulph.,  0.008  Gm.  (^  gr.) 
p.  r.  n.  (for  extreme  dyspncea). 

April  25,  7.00  p.m.  No  change  in  condition.  No  urgent  dyspnoea.  Haemoglobin 
110  per  cent.  (Dare).  Cyanosis  still  marked.  No  auricular  wave  in  venous  pulse.  Heart's 
action  still  weak  and  irregular. 

1100  c.c.  of  blood  were  then  removed  from  right  arm,  after  which 
haemoglobin  fell  to  65  per  cent.  The  right  border  of  cardiac  dulness  retreated 
1  cm.  toward  midline;  upper  border  receded  .5  cm.;  left  border  unchanged.  No  change 
in  cardiac  sounds  nor  in  pulse  tracing.  No  auricular  wave  in  venous  tracing.  Blood- 
pressure:  before  venesection,  7.00  p.m.,  maximal  107,  minimal 
87,  pulse-pressure  20,  pulse-rate  116,  pulse-pressure  X  pulse- rate  =  2320;  after  vene- 
section 8.30p.m.,  maximal  112,  minimal  92,  pulse-pressure  20,  pulse- 
rate  112,  pulse-pressure  X  pulse-rate  =  2240  (see  chart,  page  176).  Cyanosis  has,  however, 
been  replaced  by  a  healthy  color,  and  patient  feels  decidedly  better.  The  improvement 
in  this  case  is  due  entirely  to  relief  of  the  over-distended  right  heart,  partly  by  diminution 
of  fluid,  partly  by  diminution  in  the  viscosity  of  the  blood  from  the  removal  of  so  many 
blood-corpuscles. 

The  patient  passed  a  comfortable  night  and  for  several  days  felt  somewhat  better. 
The  course  of  symptoms  and  their  relation,  medication,  and  blood-pressure  changes  are 
shown  in  the  chart  (Fig.  130).  He  was  bled  (350  c.c.)  again  on  May  14,  with 
considerable  benefit,  and  from  that  time  his  condition  steadily  improved. 


240 


DISEASES   OF   THE   HEART   AND    AORTA. 


PARALLELISM    BETWEEN    MANIFESTATIONS    OF     PRIMARY    MYOCARDITIS    AND 

PRIMARY    NEPHRITIS. 

The  cases  of  chronic  myocarditis  with  arteriosclerosis  and  secondary 
renal  involvement  often  very  closely  resemble  those  of  primary  renal 
involvement  with  secondary  myocarditis,  since  there  are  both  cardiac  and 
renal  failure  in  both  conditions. 

The  following  abstracts  show  the  close  parallelism  between  the  symptoms  and  signs 
of  two  such  cases  which  in  the  early  stages  were  almost  exactly  similar: 


Chronic  myocarditis  (C.  B.).     (Diagnosis  on 
first  admission  "  chronic  nephritis  "  ). 


Chronic  nephritis  (J.  B.). 


Illness. 


Signs. 


Urine. 


Autopsy. . 


Shortness  of  breath,  palpitation,  cough, 
swelling  of  abdomen  and  legs.  Voids 
during  night. 

Pale  pasty  color.  Moist  rales  in  chest. 
Heart  dilated  to  left  (15  cm.);  rapid 
regular  pulse  120;  sclerotic  radials. 
Maximal  blood-pressure.  ISO  mm. 
Hg.  Later,  two  attacks  of  angina 
pectoris,  with  death  in  the  second. 


Varying  from  2O0O-.3000  c.c.  per  day, 
with  sp.  gr.  1007,  trace  of  albumen 
and  a  few  hyaline  casts,  to  less  than 
1700  c.c,  with  sp.  gr.  1020,  large 
amount  of  albumen,  and  numerous 
hyaline  casts. 

Heart  hypertrophied  650  Gm.,  auri- 
cles dilated;  intense  cardiosclerosis, 
with  some  llypertroph^^  Both  coro- 
nary arteries  diseased,  left  descend- 
ing branch  almost  obliterated. 

Kidneys  large,  purple,  with  a  few 
depressed  scars  and  retention  cysts; 
cortex  thicker  than  normal;  no  in- 
crease in  interstitial  tissue;  no 
marked  nephritic  changes. 

Adrenals  — fatty  degeneration  of 
cortical  cells;    no  hypertrophy. 


Shortness  of  breath,  orthopnoea,  swell- 
ing of  legs. 


Pale  pasty  color.  Moist  rales  in  chest. 
Heart  dilated  to  left  (14  cm.)  and 
right  (5  cm.).  Pulse  rapid  and 
regular.  Maximal  blood-pressure 
200  mm.  Hg;  later  ranged  from 
130  to  170  mm.  Hg.  Fundi  oculo- 
rum  normal.  Later,  Cheyne-Stokes 
breathing.  Delirium;  headache;  dul- 
ness. 

Urine  varied  from  400  c.c,  with  sp. 
gr.  1022,  2.5  Gm.  albumen  per  litre, 
and  numerous  hyaline  and  granular 
casts,  to  2500  c.c,  sp.  gr.  1007,  trace 
of  albumen,  and  few  casts. 


Heart  dilated  350  Gm.;  pale  pink 
walls,  with  slight  fibrosis.  Coronary 
arteries  sclerotic. 


Kidneys  small,  scarred,  cortex  thin; 
extensive  epithelial  degeneration 
with  corresponding  proliferation  of 
connective  tissue.  Many  glomeruli 
have  undergone  fibrosis. 


It  may  be  almost  impossible  to  establish  differential  diagnosis  between 
two  such  cases  early  in  the  disease.  The  course  of  the  two  cases,  however, 
showed  clearly  the  divergence,  the  one  toward  the  type  of  coronary  sclerosis, 
dilated  heart,  precordial  pain,  paroxysmal  dyspnoea,  the  other  toward 
the  ursemic,  with  progressive  dulness,  oliguria.  Albuminuric  retinitis  did 
not  develop  in  the  case  cited,  or  the  diagnosis  might  have  been  simplified. 

Catalase  Test. — Recent  studies  of  M.  C.  Winternitz  indicate  that  in 
many  cases  at  least  the  diagnosis  may  be  made  by  a  simple  chemical  test. 


AFFECTIONS   OF  THE   MYOCARDIUM.  241 

He  has  found  that  in  chronic  nephritis  the  catalase  of  the  blood  is  destroyed, 
so  that,  when  placed  in  contact  with  hydrogen  peroxide,  no  oxygen  is 
liberated;  while  the  blood  of  patients  with  cardiac  weakness  splits  peroxide 
as  before.  By  this  test  he  has  made  correct  diagnosis  in  a  number  of  doubt- 
ful cases.  However,  this  difference  in  the  catalase  manifests  itself  only  in 
the  uremic  and  preursemic  states  and  is  of  value  only  in  distinguishing 
between  these  conditions  and  cases  of  myocardial  weakness  with  drowsiness. 

DIAGNOSIS. 

In  making  the  diagnosis  it  is  most  important  to  differentiate  chronic 
myocarditis  from  the  following  conditions:  (1)  organic  valvular  heart 
lesions,  (2)  obesity,  (3)  primary,  cardiac  overstrain,  (4)  primary  chronic 
nephritis,  (5)  chronic  polycythsBmia  (erythraemia)  with  enlarged  spleen,  (6) 
neurasthenia  and  psychasthenia,  (7)  chronic  nephritis. 

In  cases  of  chronic  myocarditis  it  may  be  extremely  difficult  to  exclude  an 
organic  valvular  disease.  This  is  especially  true  of  mitral  insufficiency,  for 
there  is  frequently  a  fimctional  mitral  insufficiency  present  with  systolic  murmur  and 
horizontal  dilatation  of  the  heart  to  the  left.  While  it  is  true  that  the  murmur  of  a  func- 
tional mitral  insufficiency  is  rarely  as  rough  as  those  of  organic  origin  may  become,  and  is 
as  a  rule  not  as  well  transmitted  into  the  axilla,  nevertheless  in  individual  cases  these 
differences  may  not  be  striking.  Much  more  striking  are  the  changes  in  the  character  of 
the  murmur  as  the  patient's  condition  improves.  In  organic  lesions  the  murmur  will 
become  louder  as  improvement  sets  in,  because  the  heart  has  become  stronger.  In 
functional  cases,  though  it  may  become  louder  at  first,  it  will  vary  greatly  in  character 
and  in  intensity,  especially  if  the  patient  is  made  to  exercise  slightly.  It  may  show  a  ten- 
dency to  disappear  altogether  during  recovery. 

The  presence  of  a  large,  slow,  heaving  apex  beat  with  slow  pulse  and  systolic  mur- 
mur as  well  as  a  large  slow  pulse  speaks  in  favor  of  organic  mitral  insufficiency  (marked 
hypertrophy  of  the  left  ventricle),  though  a  functional  papillary  insufficiency  might  per- 
sist from  localized  myocarditis  of  one  of  the  papillary  muscles  in  spite  of  the  hypertrophy. 

From  other  valvular  diseases  the  diagnosis  is  comparatively  easy.  In 
occasional  cases  the  beat  of  the  auricle  becomes  audible,  suggesting  the  presystolic  rumble 
of  mitral  stenosis  (Sewall);  and  occasionally  blowing  diastolic  murmurs  at  the  sternal 
margin  suggest  organic  aortic  or  pulmonic  insufficiency.  But  such  dilatations  of  the  aortic 
ring  and  conus  arteriosus  or  cardiopulmonary  murmurs  are  rather  rare  and  are  usually 
transitory. 

A  functional  tricuspid  insufficiency  results  so  constantly  from  weak- 
ening of  the  right  ventricle  that  it  is  a  lesion  to  be  included  under  rather  than  excluded 
from  the  picture  of  chronic  myocarditis. 

Primary  cardiac  overstrain  may  be  excluded  through  the  history,  the 
trouble  in  the  latter  condition  coming  on  suddenly  in  a  previously  healthy  individual 
during  or  immediately  after  a  severe  strain,  while  in  chronic  myocarditis  there  is  usually 
a  more  gradual  onset  of  symptoms,  frequently  traceable  to  febrile  disease  or  intoxication. 

Obesity  is  diagnosed  from  the  general  appearance  of  the  patient,  concomitant 
chronic  myocarditis  being  excluded  when  the  trouble  seems  to  bear  a  relation  to  too  good 
health  rather  than  to  disease.    However,  myocardial  changes  may  be  very  hard  to  rule  out. 

The  differentiation  from  chronic  nephritis  has  been  discussed  above. 

Chronic  polycythaemia  (erythremia)  with  enlarged  spleen  may  present 
a  picture  very  similar  to  primary  chronic  myocarditis,  and  in  the  later  stages  a  consider- 
able grade  of  myocarditis  may  be  present.  The  size  and  hardness  of  the  spleen,  the  color, 
and  the  high  blood  count  are  the  features  upon  which  the  diagnosis  is  made. 

Neurasthenia,    cardiac    neuroses,    or    pseudocardiac    visceral    disease, 
must  be  carefully  excluded  (see  page  593).      In   the   former   the  weakness  when    self- 
conscious  and  the  strength  when  the   mind   is   distracted   are   totally  disproportionate; 
while  the  myocarditic  is  reminded  of  his  weakness  by  the  stern  hunger  for  air. 
16 


242  DISEASES   OF  THE   HEART   AND    AORTA. 

A  careful  general  examination  should  always  be  made  to  exclude  cardiac  weakness 
from  enteroptosis  and  similar  disorders  that  may  reflexly  give  rise  to  a  true  cardiac 
weakness. 

The  venous  pulse  helps  somewhat,  the  presence  of  a  visible  " single  venous 
pulse"  of  auricular  paralysis  or  extrasystoles  suggesting  myocardial  change.  However, 
these  may  not  be  conclusive.  For  the  past  year  the  writer  has  had  under  observation  a 
young  athlete  with  permanently  irregular  pulse  and  auricular  paralysis  and  symptoms  of 
slight  cardiac  weakness  on  exertion.  There  are,  however,  no  infectious  diseases  nor  indis- 
cretions to  account  for  the  production  of  a  myocarditis,  and,  though  the  writer  inclines 
toward  the  diagnosis  of  the  latter  condition,  it  seems  difficult  in  so  healthy  a  young  person 
to  exclude  a  neurotic  basis. 

TREATMENT. 

The  treatment  of  chronic  myocarditis  in  the  main  should  follow  the 
general  scheme  laid  down  in  detail  in  Chapters  IV.,  V.,  and  VI. :  re  st  in  bed 
during  the  severer  stages  of  failure,  purgation,  light  diet,  digitalis  or 
strophanthus  in  severe  cases,  graduated  resistance  exercises  and  Nauheim 
baths  during  convalescence,  gradually  increasing  walks  and  moderate 
exercise  before  returning  to  every-day  life.  However,  certain  exceptions 
must  be  noted,  especially  in  the  severer  forms  of  myocarditis.  For  example, 
digitalis  only  occasionally  corrects  an  irregularity  which  has  become 
relatively  permanent;  though  it  is  very  useful  in  curing  the  milder  forms 
of  irregularity,  such  as  a  continual  bigeminal  pulse  or  occasional  ventricular 
extrasystoles.  It  is  less,  indeed  rarely,  efficient  in  removing  the  irregulari- 
ties arising  at  the  auricles.  On  the  other  hand,  in  dealing  with  the  advanced 
grades  of  permanent  arrhythmia  with  paralysis  of  the  auricles,  where  there 
is  usually  advanced  myofibrosis  and  only  a  few  of  the  heart  muscle-cells 
have  survived  the  general  atrophy,  it  is  found  that  these  often  respond 
well  to  small  doses  (about  half  the  normal) ,  whereas  a  normal  dose 
may  give  rise  to  symptoms  of  definite  digitalis  poi- 
soning and  often  hasten  death.  This  is  not  always  to  be  avoided  by  the 
apparently  mild  routine  of  administering  the  drug  in  "courses,"  since  the 
initial  dose  may  be  too  large  for  the  individual  case.  Each  case  must  be 
considered  for  itself,  with  these  facts  constantly  borne  in  mind.  The  moder- 
ate-sized initial  dose  or  two  followed  by  prolonged  administration  of  very 
small  doses,  suggested  by  Frankel  (see  page  179),  seems  to  be  the  safest  and 
surest  method  in  these  cases,  in  order  to  prevent  cumulative  effects. 

The  recent  introduction  of  single  doses  ofstrophanthin  intra- 
venously, which  does  not  increase  peripheral  resistance,  gives  promise 
of  great  results  in  the  future,  especially  in  this  group  of  cases,  although  its 
use  has  not  yet  become  general  enough  to  warrant  a  verdict. 

As  to  graduated  exercises,  these  are  useful  in  many  cases, 
but  are  distinctly  contraindicated  after  myofibrosis  has  set  in  and  dyspnoea 
persists  while  the  patient  is  at  rest.  Mere  arrhythmia,  even  with  paralysis 
of  the  atria,  does  not  contraindicate  their  use,  but  points  a  warning,  and 
in  many  cases  shows  that  the  practitioner  is  treading  on  dangerous  ground. 
This  applies  also  to  Nauheim  and  other  baths.  Coronary  sclerosis, 
on  the  other  hand,  stenocardia,  and  severe  pains  down  the  arms  furnish 
distinct  contraindications  to  all  exercises  except  such  as  are  necessary. 
Even  those  of  Schott  must  be  carried  out  with  the  utmost  precaution,  and 
the  bending  exercises  may  well  be  eliminated.     The  walks,  etc.,  which 


AFFECTIONS   OF  THE   MYOCARDIUM.  243 

terminate  the  treatment  must  be  taken  slowly  and  with  the  greatest  pre- 
caution in  avoiding  fatigue. 

For  the  stenocardiac  attacks  and  paroxysmal  dyspnoea  the  greatest 
relief  is  given  by  a  pearl  or  two  ofamyl  nitrite  followed  by  nitro- 
glycerin and  sodium  nitrite.  Indeed,  these  drugs  furnish  a 
good  deal  of  relief  where  the  arteriosclerotic  element  is  prominent. 

When  the  blood-pressure  is  elevated  above  140  mm.  the  salt  in  the 
food  should  be  reduced  as  low  as  possible  (see  page  168). 

Venesection  may  be  of  the  greatest  value  in  tiding  over  periods 
of  acute  dilatation,  as  shown  in  the  case  of  G.  G.,  even  when,  as  in  that  case, 
it  produces  no  change  in  maximal  or  minimal  blood-pressure  or  pulse-rate.' 
This  case  also  exemplifies  the  fact  that  the  venesection  may  often  be  of 
great  benefit  before  acute  signs  of  cardiac  overfilling  set  in,  and  then  it  is 
to  be  regarded  as  "  a  stitch  in  time,"  the  relief  of  the  over-distention  enabling 
the  heart  to  right  itself.  This  may  be  owing  to  the  fact  that  the  over- 
stretched fibres  are  allowed  to  gain  their  optimum  length,  or,  on  the  other 
hand,  to  the  removal  of  a  large  number  of  red  corpuscles  from  the  circulatory 
system,  thus  decreasing  the  viscosity.  It  is  easier  to  pass  than  to  seize  the 
moment  at  which  a  venesection  would  do  most  good. 

In  this  every  one  some  day  or  other  receives  his  lesson.  For  example,  the  writer 
had  a  patient  under  his  care  in  San  Francisco  who  one  night  had  a  moderate  degree  of 
dyspnoea  and  cyanosis,  though  scarcely  enough  to  cause  alarm,  and  immediate  venesec- 
tion was  considered.  The  right  heart  was  not  markedly  enlarged  and  none  of  the  objec- 
tive signs  seemed  urgent.  It  was  decided  to  do  the  venesection  the  next  day,  and  the 
patient  was  given  fifteen  milligrams  (a  quarter  grain)  of  morphine,  after  which  he  fell 
into  a  quiet  sleep  almost  immediately.  A  couple  of  hours  later  he  became  restless  and 
sank  gradually  within  an  hour.  We  had  let  the  right  moment  for  the  venesection  pass, 
and  had  masked  the  symptoms  by  the  morphine. 

Dangers  from  Morphine. — Another  danger  due  to  morphine  lies 
in  the  danger  of  habituation  (see  page  149),  and  the  further  danger  that 
in  order  to  get  it  the  patient  will  simulate  a  paroxysm  of  dyspnoea  and 
actually  make  himself  sick  or  even  endanger  his  life  by  the  effort  entailed 
in  doing  so.  Several  patients  whom  the  writer  has  gradually  broken  of 
their  morphine  habit  confessed  to  having  done  so,  even  though  they  knew 
at  the  time  that  the  simulation  of  dyspnoea  made  them  feel  worse. 

THROMBI    IN    THE    CARDIAC   CHAMBERS. 

When  the  circulation  is  slowed,  and  especially  when  one  of  the  cardiac 
chambers  empties  itself  insufficiently,  large  clots  are  liable  to  form  along 
its  wall  (mural  thrombi).  This  occurs  especially  in  those  portions  which 
are  away  from  the  axial  stream,  such  as  the  recesses  between  the  trabeculse 
carnese  and  behind  the  papillary  muscles,  and  also  out  in  the  tip  of  the  auric- 
ular appendages. 

Thrombosis  within  the  left  auricle  occurs  quite  frequently  in  mitral  stenosis, 
especially  when  the  blood  stagnates  there  during  periods  of  overstrain.  These  thrombi 
if  fresh  sometimes  break  loose  to  form  emboli  (page  151).  Sometimes  the  clot  loosened 
from  the  auricular  appendix  is  so  large  that  it  cannot  pass  through  the  auriculoventricular 
orifice,  but  plugs  the  latter  entirely,  producing  sudden  death.  When  the  clot  remains 
adherent  to  the  wall  for  some  time,  more  or  less  organization  goes  on.     Thrombi  which 


244  DISEASES   OF  THE   HEART    AND    AORTA. 

adhere  to  the  wall  by  a  few  strands  of  newly  formed  connective  tissue  are  of  every-day 
occurrence,  and  constitute  the  classical  sign  for  differentiation  between  intra-vitain  and 
post-mortem  thrombi.  In  older  thrombi  the  organization  is  more  complete,  so  that  a 
thrombus  mass  may  adhere  to  the  cardiac  wall  by  a  pedicle  of  fibrous  tissue.  It  is  quite 
possible  that  in  some  cases  these  thrombi  vibrate  to  and  fro  and  cause  extrasystoles  by 
striking  against  the  walls  of  the  heart,  just  as  occurred  in  Cameron's  air-bubble  experi- 
ment (quoted  on  page  71).  In  several  cases  such  masses  have  been  known  to  act  as  a 
ball-valve   at  the  mitral  orifice,  giving  rise  to  signs  of  mitral  stenosis. 

The  symptoms  and  signs  given  by  such  thrombi  are,  however,  very  obscure.  The 
fact  that  they  usually  arise  during  the  course  of  a  cardiac  failure  adds  to  the  complexity 
of  the  clinical  picture,  and  the  diagnosis  can  rarely  be  made  until  embolism  sets  in. 
In  one  case  of  mitral  stenosis  recently  seen  by  the  writer,  in  which  the  whole  descending 
abdominal  aorta  was  suddenly  plugged  by  an  embolus  and  gangrene  of  both  lower  extremi- 
ties set  in,  the  diagnosis  of  a  clot  within  the  heart  was  warrantable.  Such  cases  are,  how- 
ever, rare,  and  the  diagnosis  is  then  made  after  the  harm  has  been  done. 

TUBERCULOSIS  OF  THE  HEART. 

In  spite  of  the  great  frequency  with  which  tuberculosis  affects  the  lungs,  pleura,  and 
pericardium,  independent  affection  of  the  myocardium,  endocardium,  and  valves  is  quite 
infrequent.'  Thus  Willigk  found  only  2  cases  of  tubercle  of  the  myocardium  in  1845 
autopsies  on  persons  with  tuberculosis.     Other  observers  confirm  this  view  of  its  rarity. 

Pathologically  the  lesions  in  tuberculosis  of  the  myocardium  resemble  those  of  tuber- 
cles elsewhere;  they  are  somewhat  more  common  in  acute  miliary  tuberculosis  than  in 
the  chronic  form,  but  in  the  latter  are  larger  in  size.  The  most  common  cardiac  lesion  of 
tuberculosis  is,  however,  neither  miliary  nor  large  solitary  tubercles,  but  a  fatty  degener- 
ation of  the  myocardium,  due  in  part  to  the  anaemia  and  in  part  to  the  toxins  secreted 
by  the  bacilli. 

The  effect  of  the  tuberculous  lesions  upon  the  circulation  is  usually  masked  by  the 
general  cardiac  weakness  due  to  the  intoxication  and  anaemia,  and,  as  v.  Leyden  states, 
does  not  present  any  characteristic  features.  It  is  almost  impossible  to  diagnose  clinically, 
for  the  symptoms  and  signs  are  quite  independent  of  the  tubercle.  Often,  as  in  Pollak's 
case,  a  man  of  65  who  had  a  large  tubercle  in  the  wall  of  the  auricle,  there  are  no  signs  what- 
ever, even  of  cardiac  weakness.  V.  Tabora  and  Tilp  report  a  case  in  which  a  systolic  mur- 
mur was  heard  over  the  apex,  but  this,  of  course,  presents  nothing  characteristic  and  might 
well  have  been  due  to  the  accompanying  weakness  of  the  myocardium  or  papillary  muscles. 
Indeed,  as  Romberg  states,  tuberculosis  of  the  myocardium  interests  the  pathologist  rather 
than  the  clinician. 

SYPHILIS  OF  THE  MYOCARDIUM. 

Syphilitic  affection  of  the  heart  is  more  frequent  and  presents  a  somewhat  more 
definite  picture  than  tuberculosis.  The  most  common  form  in  which  syphilis  affects  the 
heart  is  the  sclerotic  lesion  of  the  aortic  valves  (see  page  361),  though 
in  this  case  the  pathological  process  originates  in  the  aorta  rather  than  in  the  myocardium. 

Grassmann  has  called  attention  to  the  frequency  with  which  signs  of  severe  cardiac 
weakness  occur  during  the  secondary  stage  of  syphilis,  accidental  or  functional 
systolic  nmrmurs  being  present  in  40  per  cent,  of  his  cases.  Dilatation,  especially  of  the 
right  heart,  was  common,  as  well  as  alterations  of  rhythm, — sometimes  arrhythmia, 
sometimes  bradycardia,  sometimes  tachycardia.  Precordial  pain  and  anginal 
attacks  were  frequent.  The  blood-pressure  was  usuafly  low,  as  was  also  the  haemoglobin. 
It  is  not  impossible  that  the  major  role  in  many  of  these  cardiac  manifestations  is  played 
by  the  anaemia  and  the  fever  rather  than  by  spirochaete  pallida  within  the  heart  muscle; 
but  the  presence  of  tertiary  myocardial  lesions  demonstrates  that  the  latter  play  an  im- 
portant part.  The  diagnosis  is  based  upon  the  above-mentioned  symptoms  arising 
during  the  secondary  stage.  Treatment  should,  of  course,  be  vigorous,  and  as  a  precau- 
tionary measure  the  patient  should  be  kept  in  bed  until  all  cardiac  weakness  has  passed. 
If  the  symptoms  do  not  rapidly  subside,  a  few  doses  of  digitalis  or  strophanthus  may  be 

*  Tuberculous  endocarditis  is  discussed  on  page  303. 


AFFECTIONS   OF  THE   MYOCARDIUM.  245 

given.  Indeed,  a  few  small  doses  of  one  of  these  drugs  may  well  be  given  to  relieve  promptly 
the  dilatation  and  thus  to  forestall  the  danger  that  may  lurk  in  an  oedematous  heart  muscle 
(see  page  235). 

Cardiac  lesions  are  rather  common  in  congenital  syphilis,  though  this  is 
not  true  of  typical  gummata.  Thus  Mracek  found  myocardial  changes  (acute  myocarditis 
with  patches  of  perivascular  infiltration  of  mononuclear  cells)  present  in  24  out  of  150 
autopsies  upon  syphilitic  foundlings,  but  gummata  in  only  4.  The  non-gummatous 
changes  are  well  described  by  I.  Adler  as  infiltrations  of  mononuclear  cells  about  the 
blood-vessels  and  in  the  connective-tissue  septa  between  the  muscle-fibres.  The  striking 
feature  is  early  typical  chronic  endarteritis  with  thickening  of  the  intima,  destruction  of 
the  elastica  internk.  This  is  often  accompanied  by  hemorrhages  into  and  about  the  vessel 
wall.  Clinically  hereditary  lues  of  the  myocardium  probably  cooperates  with  the  other 
syphilitic  lesions  in  bringing  about  the  death  of  the  child,  but  the  importance  of  its  role 
cannot  be  judged,  since  it  is  rarely  if  ever  the  only  luetic  lesion  present. 

The  tertiary  myocardial  lesions  of  adults  are  fairly  common.  The  lesions 
in  60  cases  collected  by  Mracek  showed  the  following  distribution:  gummatous  myocar- 
ditis, 10;  fibrous  myocarditis,  9;  gummatous  and  fibrous,  8;  endocarditis,  2;  coronary 
arteries  alone,  3;  pericardium  alone,  1;  myocardium  and  pericardium,  15;  pericardium, 
myocardium,  and  endocardium,  1;  myocardium  and  coronary  arteries,  1;  all  parts  of  the 
heart,  6;  cardiac  ganglia,  4. 

Judging  by  the  number  of  cases  of  Adams-Stokes  syndrome  due  to 
lues  (see  page  471),  the  intraventricular  septum  seems  to  be  a  rather  frequent  site  for 
the  lesions.  Excepting  such  lesions  as  are  so  situated  that  they  give  rise  to  heart-block 
or  to  the  Adams-Stokes  syndrome,  the  syphilitic  lesions  of  the  myocardium  rarely  give 
distinct  manifestations.  A  general  myocardial  weakness,  shortness  of  breath,  dilatation 
with  or  without  exertion  in  persons  who  have  had  lues  (especially  with  other  visceral 
involvement)  is  suggestive  evidence  of  fibrous  luetic  myocarditis  with  or  without  gumma. 
The  latter  can  rarely  if  ever  be  diagnosed.  Huchard  and  Fiessinger  report  a  case  in  which 
dyspnoea  set  in  suddenly  15  days  before  death,  due  to  the  growth  of  a  gumma  involving 
the  tricuspid  valve,  but  even  in  such  a  case  the  data  are  too  uncertain  to  permit  a  definite 
clinical  diagnosis.  A  positive  Wassermann  reaction,  which  Collins  and 
Sachs  and  W.  Longcope  have  found  so  useful  in  the  diagnosis  of  luetic  aortic  insufficiency, 
is  of  less  value  in  the  diagnosis  of  luetic  myocarditis,  since  the  evidences  of  myocarditis 
are  in  themselves  less  definite.  However,  in  cases  of  chronic  myocardial  weakness  in  which 
lues  is  suspected,  the  presence  of  a  positive  Wassermann  reaction  renders  a  vigorous  ad- 
ministration of  mercurial  inunctions  or  hypodermic  injection  of  mercurial  salts,  as  well 
as  vigorous  doses  of  potassium  iodide,  highly  advisable.  In  occasional  cases  it  may  be 
possible  to  secure  a  considerable  and  permanent  improvement  by  vigorous  antiluetic 
treatment,  even  when  the  Adams-Stokes  syndrome  is  present;  but  it  must  not  be  forgotten 
that  the  cardiac  infiltrations  are  among  the  most  stubborn  of  all  luetic  lesions. 

TUMORS  OF  THE  HEART. 

Primary  tumors  of  the  heart  are  so  rare  that  in  3000  consecutive  autopsies  at  Niirn- 
burg  Thorel  did  not  encounter  a  single  one,  and  Hektoen,  who  reported  three  cases  in  1893, 
states  that  reports  of  only  110  cases  of  cardiac  tumors  were  to  be  found  in  the  Index  Cata- 
logue of  the  Surgeon-General's  Library,  and  most  of  these  were  secondary. 

Primary  Tumors. — Bertheson  was  able  to  collect  28  primary  tumors  of  the  following 
types:  sarcoma  9;  myxoma  7;  fibroma  6;  carcinoma  3;  Hpoma  2;  cystoma  1.  Link 
(1909)  has  recently  collected  the  data  of  91  cases;  61  of  these  were  as  follows:  carcinoma 
7;  fibroma  7;  myoma  5;  lipoma  8;  sarcoma  13;  myxoma  18;  rhabdomyoma  1;  tera- 
toma 1;  papilloma  1.  In  addition  to  these  Knox  and  Schorer  and  Wolbach  have  collected 
12  cases  of  rhabdomyoma;  6  of  which  were  associated  with  other  malformations,  especially 
cerebral  sclerosis  and  hydrocephalus. 

Hektoen  calls  attention  to  the  fact  that  the  heart,  and  hence  also  its  primary  tumors, 
are  of  mesoblastic  origin;  which  accounts  for  the  relative  rarity  of  primary  car- 
cinomata  and  the  preponderance  of  sarcomata.  Thorel  believes  that  many  of  the  fibro- 
mata found  represent  merely  old  organized  thrombi  clinging  to  the  heart  wall,  and  believes 
that  many  of  the  (relatively  frequent)  myxomata  represent  merely  degenerating  forms  of 


246  DISEASES   OF   THE   HEART   AND    AORTA. 

such  thrombi.  The  Hpomata  he  regards  merely  as  abnormally  large  pockets  of  epicardial 
or  intramural  fat  rather  than  as  true  tumors. 

As  regards  site,  Link  found  in  right  auricle  10;  left  auricle  24;  right  ventricle  14; 
left  ventricle  8;  valves  16;  interauricular  septum  2. 

Metastatic  Involvement  of  the  Heart.^Secondary  neoplasms  affecting  the  heart  are 
somewhat  more  common,  and  scarcely  any  pathologist  of  experience  has  failed  to  meet 
with  them,  especially  in  cases  with  multiple  metastasis.  Of  the  metastatic  neoplasms 
carcinomata  are  the  most  frequent.  Thorel  encountered  6  instances  in  his  3000  autopsies, 
the  primary  sites  being  uterus  2,  rectum  1,  gall-bladder  1,  kidney  1,  lung  1. 

Geipel  stated  that  in  a  series  of  16  cases  of  carcinoma  of  the  oesophagus  6  gave  metas- 
tases to  the  heart;  but  this  is  an  unusually  high  percentage,,  and  Thorel  from  his  experi- 
ence does  not  regard  such  oesophageal  tumors  as  especially  liable  to  cardiac  metastases. 

Clinically  the  presence  of  a  tumor  in  the  heart  in  itself  exerts  little  influence,  unless, 
as  in  Luce's  case  of  sarcoma,  it  presses  upon  the  auriculoventricular  bundle  and  produces 
heart-block,  or  it  is  so  situated  as  to  produce  either  stenosis  or  regurgitation  at  a  valvular 
orifice.  The  benign  tumors  exert  little  or  no  effect  upon  the  force  or  rhythm  of  the  heart; 
the  malignant  tumors  give  rise  merely  to  signs  of  cachexia  in  which  the  cardiac  weakness 
seems  incidental  rather  than  primary.  In  cases  of  generalized  carcinosis  and  sarcomatosis, 
those  in  which  the  metastatic  nodules  are  most  common,  the  cachectic  myocardial  weak- 
ness is  still  more  intense  whether  the  tumors  affect  the  heart  or  not.  The  accidental  finding 
of  a  loud  harsh  murmur  suddenly  developing  and  progressing  with  the  metastasis  elsewhere 
in  the  body  is  very  suggestive;  but  this  is  rarely  encountered. 

In  some  cases  in  which  the  tumors  are  superficial,  pericarditis  may  set  in.  Effu- 
sion, especially  blood-stained,  is  rather  comm6n  under  these  conditions 
and  the  signs  of  the  latter  may  be  the  first  and  only  sign  of  the  condition. 

In  1905  the  writer  aspirated  a  pericardial  exudate  which  contained  10  per  cent,  of 
hsemoglobin  and  some  methsRmoglobin.  The  patient  died  the  next  day,  and  autopsy 
revealed  carcinomatous  masses  in  the  myocardium  wall  and  pericardium,  which  were 
metastases  from  a  very  small  primary  carcinoma  of  the  bronchus  quite  unsuspected  during 
life.    The  finding  of  tumor  cells  in  such  an  exudate  would,  of  course,  give  the  diagnosis. 

Tumors  of  the  heart,  even  if  diagnosed,  would,  of  course,  be  inoperable. 

BIBLIOGRAPHY. 

Myocarditis. 

Sobernheim:  Praktische  Diagnostik  der  innere  Krankheiten,  Berl.,  1837. 

Boettcher,  A.,  and  Zenker.     Quoted  from  Krehl. 

Cullen,  E.  K.:  So-called  Spontaneous  Focal  Myocarditis  and  the  Occurrence  of  Calcifi- 
cation of  the  Degenerate  Muscle  Fibres,  Bull.  Johns  Hospkin  Hosp.,  Bait.,  1906,  xvii, 
267. 

Dietrich:  Die  Querlinien  des  Herzmuskels,  Verh.  d.  Deutsch.  pathol.  Gesellsch.,  Jena, 

1906,  X,  40. 

Buhlig,  W.  H.  :  A  Preliminary  Note  upon  Certain  Mechanical  Microtechnical  Factors 
Concerned  in  the  Production  of  the  Segmentation  and  Fragmentation  of  the  Myo- 
cardium, J.  Med.  Research,  Bost.,  1902,  ii,  428. 

Krehl,  L.:  Beitrag  zur  Pathologie  der  Herzklappenfehler,  Deutsch.  Arch.  f.  klin.  Med., 
Leipz.,  1890,  x\vi,  454.  Beitrag  zur  Kenntniss  der  idiopathischen  Herzmuskeler- 
krankungen,  ibid.,  1891,  xlviii,  414.  Clinical  pathology  (transl.  by  A.  W.  Hewlett), 
Phila.,  ,1905. 

Romberg,  E.:  Ueber  die  Erkrankungen  des  Herzmuskels  bei  Typhus  abdominalis,  Schar- 
lach  und  Diphtheric,  Deutsch.  Arch.  f.  klin.  Med.,  Leipz.,  1891,  xlviii,  369. 

Aschoff,   L.:  Zur  Myokarditisfrage,  Verh.  d.  Deutsch.  pathol.  Gesellsch.,   1904,  viii,  46. 

Geipel,  P.:  Untersuchungen  ueber  rheumatische  Myokarditis,  Deutsch.  Arch.  f.  klin.  Med., 
Leipz.,  1906,  Ixxxv,  75. 

Coombs,  C. :  The  Myocardial  Lesions  of  .Acute  Rheumatic  Infection,  Brit.  M.  J.,  Lond., 

1907,  ii,  1513.     Rheumatic  Myocarditis,  Quart.  J.  Med.,  Oxford,  1908-9,  ii,  26. 
Bracht,  E.,  and  Wachter:  Beitrage  zur  Aetiologie  und  pathologischen  Anatomie  der  Myo- 
carditis rheumatica,  Deutsch.  Arch.  f.  klin.  Med.,  Leipz.,  1909,  xcvi,  493. 

Cole,  R.  I.,  1.  c.,p.  320. 


AFFECTIONS   OF  THE   MYOCARDIUM.  247 

Freund,  G.:  Zur  Kenntniss  der  acuten  diffusen  Myocarditis,  Berl.  klin.  Wchnschr.,  Berl., 

1898,  XXV,  1077. 

Pearce,  R.  M.:  Experimental  Myocarditis;   a  Study  of  the  Histological  Changes  following 

Intravenous  Injections  of  Adrenalin,  J.  Exper.  Med.,  N.  York  and  Lancaster,  1906, 

viii,  400. 
Fleischer,  M.  S.,  and  Loeb,  Leo:  Experimental  Myocarditis,  Arch.  Intern.  M.,  Chicago, 

1909,  ii,  78. 
De  la  Camp,  Moritz,  Dietlen,  Hornung.    See  Chapter  on  the  Physiology  of  Cardiac  Over- 
strain. 
Roily,  F.:  Ueber  die  Wirkung  des  Diphtheriegiftes  auf  das  Herz,  Arch.  f.  exper.  Pathol,  u. 

Pharmakol.,  Leipz.,  1899,  xlii,  283. 
V.  Stejskal,  K.  Ritter  :  Kritsch-experimentelle  Untersuchungen  ueber  den  Herztod  in 

Fogle  von  Diphtherietoxin,  Part  I,  Ztschr.  f.  klin.  Med.,  Berl.,  1902,  xliv,  367;    Part 

II,  ibid.,  1904,  li,  129. 
Mackenzie,  J.:  New  Methods  in  the  Study  of  Affections  of  the  Heart,  Brit.  M.  J.,  Load., 

1905,  i,  521. 
Hibbard,  C.  M.:  Heart  Complications  in  Diphtheria,  M.  and  S.  Rep.,  Bost.  City  Hosp., 

Bost.,  1898. 
Forster,  Fr.:  Ueber  Myokarditis  und  Gefasserkrankungen  im  Kindesalter  insbesondere 

nach  akuten  Infektionskrankheiten,  Deutsch.  Arch.  f.  klin.  Med.,  Leipz.,  1906,  Ixxxv, 

35. 
Hallwachs:  Ueber  die  Myocarditis  bei  Diphtheric,  Deutsch.  Arch.  f.  klin.  Med.,  Leipz., 

1899,  Ixiv,  770. 

Ziegler,  E.:  Lehrbuch  der  Pathologie  und  der  pathologischen  Anatomic,  9th  ed.,  Jena, 

1898. 
Huchard,  H.:  Etude  clinique  de  la  cardio-sclerose,  Rev.  de  med.,  Par.,  1892,  xii,  421. 
Dehio,  K.:  Myofibrosis  cordis,  Deutsch.  Arch.  f.  khn.  Med.,  Leipz.,  1899,  Ixii,  1. 
Radasewsky:  Ueber  die  Muskelerkrankungen  der  Vorhofe  des  Herzens,  Ztschr.  f.  klin. 

Med.,  Berl.,  1895,  xxvii,  529. 
Albrecht,  E.:  Der  Herzmuskel  und  seine  Bedeutung  fiir  die  pathologische  Physiologie 

und  Klinik  der  Herzens,  Berl.,  1903. 
Aschoff,    L.,  and  Tawara,  S.:  Die   heutige   Lehre  von  den    pathologisch-anatomischen 

Grundlagen  der  Herzschwache,  Jena,  1906. 
Mackenzie,  Keith,  Wenckebach,  Schonberg.    Quoted  on  p.  15. 
Saigo:  Purkinjeschen  Muskelfasern  bei  Erkrankungen  des  Myokards.    Verhandl.  d.  deutsch. 

path.  Gesellsch.,  Jena,  1908,  xii,  165. 
Hering,  H.  E. :  Ueber  kontinuerliche  Herzbigeminie,  Deutsch.  Arch.  f.  klin.  Med.,  Leipz., 

1904, Ixxix,  175. 
Marey,  E.  J.:  La  circulation  du  sang  a  I'etat  physiologique  et  dans  les  maladies,  Paris, 

1881. 
Knoll,  Ph.:  Ueber  die  Veranderungen  des  Herzschlages  bei  reflectiorischer  Errazung  des 

vasomotischen  Nervensystems;    sowie  bei  Stiegerung  des  intracardial  Drucks  ueber- 

haupt,  Sitzungsber.  d.  k.  Akad.  d.  Wissensch.,  Wien,  Abth.  Ill  (Phvsiol.  Anat.  u. 

Med.),  1872,  Ixv-lxvi,  195. 
Hering,  H.  E.:  Ueber  die  haufige  Kombination  von  Kammervenenpuls  mit  Pulsus  irreg- 
ularis perpetuus,  Deutsch.  med.  Wchnsch.,  Leipz.,  1906,  xxxii,  1. 
Gerhardt,  D.:  Arhythmia  perpetua  des  Pulses,  Deutsch.  med.  Wchnschr.,   1907,  xxxiii, 

448. 
Thebpold,  J.:  Ein  Beitrag  zur  Lehre  von  der  Arhythmia  perpetua,  Deutsch.  Arch.  f.  klin. 

Med.,   Leipz.,    1907,   xc,   77. 
Hewlett,  A.  W.:  The  Interpretation  of  the  Positive  Venous  Pulse,  J.  Med.  Research, 

Bost.,  1907,  xvii,  119. 
Mackenzie,  James,  and  Gibson,  G.  A.    Quoted  on  p.  78. 

Tuberculosis  of  the  Myocardium. 

Pollak,  S.:  L'^eber  Tuberculose  des  Herzmuskels,  Ztschr.  f.  klin.  Med.,  Berl.,  1892,  xxi,  185. 
Brosch,  A.:  Ein  Fall  von  Herztuberkulose  mit  typischen  Weilschen  Symptomenkomplex, 
Wien.  med.  Pr.,  1896,  xxxvii,  985. 


248  DISEASES   OF   THE   HEART   AND   AORTA. 

V.  Leyden,  E.:  Ueber  die  Affection  des  Herzens  mit  Tuberculose,  Deutsche  med.  Wchn- 

schr.,  Leipz.,  1896,  xxii,  1. 
V.  Tabora  and  Tilp:  Zur  Kasuistik  der  Herztuberkulose,  ibid.,  1908,  xxxiv,  Vereinsbeil  805. 

Cardiac  Syphilis. 

Grassmann:  Ueber  acquerirte  Syphilis  des  Herzens,  Miinchen.  med.  Wchnschr.,  1897, 
xliv,  473,  506,  522.  Klinische  Untersuchungen  an  den  Kreislauforganen  im  Fruh- 
stadium  des  Syphilis,  Deutsches  Arch.  f.  klin.  Med.,  Leipz.,  1900,  Ixix,  58,  264. 

Mracek,  F. :  Die  Syphilis  des  Herzens  bei  erworbener  und  ererbter  Lues,  Arch.  f.  Dermatol, 
u.  Syph.,  Wien  and  Leipz.,  1893,  xxv  (Erganzungshefte),  p.  279. 

Adler,  I.:  Observations  on  Cardiac  Syphilis,  Trans.  Assoc.  Am.  Phys.,  Phila.;  1898,  xiii, 
73;  and  N.  York  M.  J.,  1898,  Ixviii,  577. 

Sacharjin:  Die  Lues  des  Herzen  von  der  klinischen  Seite  betrachtet,  Deutsches  Arch.  f. 
klin.  Med.,  Leipz.,  1889,  xlvi,  388. 

Le  Count,  E.  R.:  Gummata  of  the  Heart  in  a  Case  of  Congenital  Syphilis,  J.  Am.  M.  Assoc, 
Chicago,  1898,  xxx,  181. 

Huchard,  H.,  and  Fiessinger:  Syphilis  gommeuse  du  coeur.  Rev.  de  M^d.,  Par.,  1907,  xxvii. 

Tumors  of  the  Heart. 

Thorel,  C:  Pathologie  der  Kreislaufsorgane,  Ergebn.  d.  allg.  Path.  u.  path.  Anat.  d.  Mensch. 

u.  d.  Tiere,  herausg.  v.  Lubarsch  u.  Ostertag.,  Wiesb.,  1903,  ix,  1  Part;    and  1907, 

xi,  Pt.  2.    With  excellent  bibliography. 
Hektoen,  L.:  Three  Specimens  of  Tumors  of  the  Heart,  etc.,  Med.  News,  Phila.,  1893, 

Ixiii,  571. 
Berthenson,  L.:  Zur  Frage  von  der  Diagnose  primarer  Neoplasmen  des  Herzens,  Myxom 

des  linken  Vorhofs,  Arch.  f.  path.  Anat.,  etc.,  Berl.,  1893,  cxxxii,  390. 
Link  R.:  Klinik  der  primarer  Neubildungen  des  Herzens,  Ztschr.  f.  klin.  Med.,   Berl., 

1909,  Ivii,  272. 
Knox,  J.  H.  M.,  and  Schorer,  E.:  A  Multiple  Rhabdomvoma  of  the  Heart  Muscle,  Arch. 

Ped.,  N.  York,  1906. 
Wolbach,  S.  B.:  Congenital  Rhabdomyoma  of  the  Heart,  J.  Med.  Research,  Bost.,  1907, 

xvi,  495. 
Geipel.     Quoted  from  Thorel. 
Luce.     Quoted  on  p.  478. 


X. 

ARTERIOSCLEROSIS. 

NORMAL    CHANGES    IN    THE    ARTERIES    DURING    LIFE. 

A  certain  degree  of  progressive  change  in  the  walls  of  the  arteries 
occurs  normally  throughout  life,  and  is  therefore  not  to  be  considered 
pathological.  The  condition  of  the  arteries  normal  to  a  man  of  thirty 
would  be  thoroughly  abnormal  in  a  child,  and  those  normal  for  a  man  of 
seventy  would  in  turn  be  regarded  as  abnormal  in  a  man  of  forty. 

Thus,  Thayer  and  Fabyan  state  that  "at  birth  the  artery  (radial)  is  deHcate, 
translucent,  extremely  thin,  and  collapsing.  The  surface  on  opening  is  perfectly  smooth. 
The  i  n  t  i  m  a  consists  of  a  single  endothelial  layer  lying  directly  on  the  surface  of  a  deeply 
undulating  elastica  interna.  The  media,  which  consists  of  transversely  arranged  smooth 
muscle-fibres  with  rather  large  vesicular  nuclei,  has  a  depth  of  seven  to  eight  layers  of  cells. 
Connective  tissue,  if  present  in  the  intima  and  media,  is  extremely  scanty,  none  being 
revealed  by  the  Mallory  or  Van  Gieson  stains.  There  is,  however,  a  relatively  large  amount 
of  elastic  tissue  which  appears  on  cross  section  as  very  thin,  parallel,  slightly  wavy  lines. 
The  elastica  externa  is  neither  as  coarse  nor  as  deeply  undulating  as  the  interna. 

"The  adventitia,  considerably  thicker  than  the  media,  consists  of  compact  con- 
nective-tissue fibres  with  relatively  large  nuclei.    The  elastic  fibres  are  fairly  numerous. 

"  By  the  middle  of  the  first  decade,  the  intima  has  become  thicker  owing  to  the  appear- 
ance of  a  fresh  layer  of  elastica  interna,  while  more  muscle-fibres  appear  in  the  media. 

"10-20  years.  Walls  of  the  vessel  become  thicker  but  still  collapsed.  Intima 
and   media   thicker,    the  elastic  tissue  being  relatively  less  marked. 

"21^0  years.  Slight  further  general  thickening  of  intima  and  media.  A  sec- 
ond elastic  layer  appears  in  the  intima.  In  the  media  the  connective  tissue  begins 
to  be  demonstrable  by  Van  Gieson's  stain. 

"  41-50  years.  Decided  change.  Lumen  of  the  vessel  remains  open.  Areas  of 
calcification  in  the  deep  layers  of  the  intima  are  frequent.  The  media  reaches  its 
maximum  thickness.    There  is  a  good  deal  of  connective  tissue. 

"After  the  fifth  decade  there  is  a  progressive  increase  in  the  thickness  of  the  intima 

....  and  a  diffuse  connective-tissue  thickening  becomes  the  common  type The 

media  after  the  fifth  decade  becomes  on  the  whole  rather  thinner;  there  is  a  marked 
increase  in  the  connective  tissue. 

"Calcification  in  the  deep  layers  of  the  intima  becomes  more  common  with 
age,  four  out  of  five  cases  in  the  eighth  and  ninth  decade  showing  this  change." 

PATHOLOGICAL    ANATOMY. 

Theoretical  Considerations.  —  Pathologically,  arteriosclerosis  is  char- 
acterized by  the  occurrence  of  changes  in  and  thickening  of  the  intima, 
which  was  supposed  by  Rokitansky  to  be  due  to  the  depositing  of  cells 
directly  from  the  blood  stream;  by  Virchow  to  be  a  true  inflammatory 
hyperplasia  as  the  result  of  some  "formative  stimulus";  and  by 
Thoma  to  be  a  compensatory  thickening  of  the  wall  in  order  to 
diminish  the  lumen  of  the  vessel  after  the  stretching  which  occurred  under 
the  increased  blood-pressure  with  which  it  was  usually  associated.  Jores,  on 
the  other  hand,  regards  this  as  a    true    hyperplasia    resulting  from 

249 


250  DISEASES   OF   THE   HEART   AND    AORTA. 

the  hio-h  blood-pressure  but  independent  of  the  lumen  of  the  vessel,  return- 
ing to  a  certain  degree  to  the  view  of  Virchow.  These  observers  con- 
sidered the  changes  in  the  intima  as  primary,  and 
tended  rather  to  neglect  the  second  important  change  which  characterizes 
arteriosclerosis,  namely  inflammatory  changes  within  the  media. 

On  the  other  hand,  Koster  and  his  pupils  called  attention  to  the  im- 
portance of  degenerative  and  calcareous  changes  in 
the  media  and  adventitia  as  well  as  in  the  intima.  Koster 
studied  the  inflammatory  process  very  carefully  by  means  of  serial  sections 
and  injected  specimens,  and  claimed  that  the  arteriosclerotic  lesion  always 
took  its  origin  in  the  adventitia  as  an  infiltration  surrounding 
the  vasa  vasorum  like  a  sleeve.  This  infiltration  followed  the 
vasa  vasorum  into  the  media.  Koster  found  that  in  the  normal  artery 
the  vasa  vasorum  do  not  pass  deeper  than  the  outer  third  of  the  media, 
though  in  certain  arteries  (notably  those  of  the  brain  and  the  lungs)  there 
was  a  fine  capillary  network  penetrating  the  deeper  layers  of  the  media  as 
well  and  spreading  along  the  medial  surface  of  the  elastica  interna. 

Changes  in  Vasa  Vasorum.  —  This  view  is  confirmed  by  v.  Ebner 
(in  Kolliker's  Handbuch  der  Gewebelehre),  who  states  that  "the  media 
of  the  larger  arteries  and  veins,  according  to  the  consensus  of  opinion 
of  many  authors,  contains  blood-vessels,  though  in  small  numbers  and  only 
in  the  external  layers;  whereas  the  inner  layers  of  the  media  and  the  intima 
seem  to  be  always  free  from  vessels  (in  the  ox  the  wall  of  the  vena  cava  is 
richly  supplied  with  vessels  even  down  to  the  intima) . 

The  infiltration  about  the  vasa  vasorum  follows  these  paths,  setting  up  areas  of 
infiltration,  necrosis,  and  calcification  in  the  smooth  muscle  and  elastic  fibres  of  the  media. 
When  it  penetrates  to  the  elastica  interna  a  small  area  of  this  is  first  injured,  the  inflamma- 
tion acts  as  a  stimulus,  and  hyperplasia  of  the  intima  sets  in.  The  intima  becomes  thick- 
ened until  its  cells  undergo  spontaneous  fatty  degeneration,  after  which  they  either  calcify 
or  the  capillary  network  penetrates  through  the  elastica  interna  and  a  true  process  of  organ- 
ization and  proliferation  of  connective  tissue  goes  on. 

Koster  admits  that  it  is  possible  that  the  degenerative  and  hyperplastic  changes  in 
the  intima  may  go  on  without  the  entrance  of  blood-vessels,  as  do  those  seen  in  inflamma- 
tions of  the  cornea;  but  he  states  that  if  the  lesions  are  followed  in  serial  sections  there 
is  almost  always  a  demonstrable  continuity  between  the  patches  of  endarteritis,  mesar- 
teritis,  and  periarteritis. 

The  number  and  size  of  the  vasa  vasorum  and  the  richness  of  the  capil- 
lary network  are  always  increased  in  arteriosclerosis  and  in  phlebosclerosis. 
He  states  that  endarteritis  occurs  only  in  arteries  that  have  vasa  vasorum, 
that  is,  in  the  larger  arteries  and  in  the  smaller  arteries  of  the  brain  and 
the  lungs. 

Koster's  version  is  extremely  fascinating,  especially  since  it  presents  a 
simple  explanation  of  a  complex  picture,  and,  on  the  other  hand,  presents 
a  clear  analogy  with  the  processes  involved  in  myocarditis,  endocarditis, 
and  other  lesions.  As  far  as  the  media  and  adventitia  are  concerned  his 
findings  have  been  confirmed  by  Ophiils,  whose  careful  study  constitutes 
one  of  the  most  important  and  clearest  of  the  recent  contributions  to  the 
subject.  Ophiils,  however,  was  unable  to  demonstrate  any  constant  rela- 
tion between  lesions  in  the  media  and  tho.se  in  the  intima,  and  beheves  that 
they  are  produced   independently  though  from  the  same  general  cause. 


ARTERIOSCLEROSIS.  251 

He  states  that  "anatomically  arteriosclerosis  of  the  aorta  is  a  unit.  It  is 
a  chronic  inflammatory  process  of  the  vessel  wall  which  attacks  all  the  coats 
simultaneously,  which  as  a  rule  first  produces  changes  in  the  intima  and 
adventitia."  He  believes  therefore  that,  as  Koster  suggested,  the  changes 
in  the  intima  begin  as  parenchymatous  changes  without  the  presence  of 
blood-vessels,  like  the  inflammations  within  the  cornea. 

CLASSIFICATION    OF    ARTERIOSCLEROTIC    LESIONS. 

Following  this  view  in  adopting  a  pathological  classification,  one  might 
distinguish  the  following  groups  of  arteriosclerotic  lesions,  dependent  upon 
the  arterial  coat  most  affected  and  the  distribution  of  the  lesions  within 
that   coat. 

...r.,.M,..  PERIARTERITIS  WOOM 

ANEURISM 
THROMBIWIGITliOBUTlRAHS  [J([)ARTERIII5  0BUTERAN5      EKDARTER1TI5  -..^^rs^^         ME5ARTERITI5 


w 

Fig.  153. — Various  types  of  arteriosclerotic  lesions.     (Schematic.) 

I.  Adventitia   chiefly  affected  (no  weakening  of  arterial  wall). 

1.  Localized   or  nodular  infiltrations  (periarteritis  nodosa). 

2.  Diffuse   infiltrations  about  the  vasa  vasorum  (causing  uniformly  thick- 

ened arteries  which  give  the  sensation  of  thick  rubber  tubing). 

II.  Lesions   in   the   media   predominate    (with   weakening    of    the    arterial   wall), 

especially  common  in  syphilis. 
L  Localized   necrosis    of    elastic    tissue   with  calcification 
(atheroma)    (pipe-stem  or  "goose-neck"  arteries,   Monckeberg's  arterio- 
sclerosis, experimental  toxic  arteriosclerosis). 
2.  Diffuse   or  patchy  medial   fibrosis  with  more   or  less   calcifica- 
tion,  often  leading  to  aneurism. 

III.  Changes   in   the    intima    predominate  (with   no  weakening   of  arterial  wall). 

1.  Hyperplasia  of  intima  with  fatty  degeneration  at  its  centre  (acute  aortitis), 

(a)  without,  (b)  with  calcification  of  the  areas  of  fatty  degeneration  (athero- 
matous plaque  or  "ulcer,"  "endarteritis  deformans,"  Longcope). 

2.  Simple   hyperplasia   of   intima    (diffuse   endarteritis)  with  increase   of 

elastic  fibres,  finally  leading  to 

3.  Obliterative   endarteritis,   in   which    the    process    is    still   more 

chronic  and  intense  and  capillaries  enter  from  the  vasa  vasorum. 

According  to  Weiss  and  v.  Winiwarter,  and  later  Buerger,  this  last  is  to  be  sharply 
differentiated  from  thromboangitis  obliterans,  in  which  intravascular  co- 
agulation precedes  or  is  independent  of  the  change  in  the  intima,  in  which  the  lumen  of 
the  vessel  finally  becomes  obliterated  by  secondarily  forming  granulation  tissue  devoid 
of  elastic  fibres  and  arising  from  about  the  newly  formed  ends  of  the  vasa  vasorum. 

Periarteritis  nodosa  (Kussmaul  and  Maier)  (supra-arterial  fibroid 
nodules),  one  of  the  rarer  forms  of  arteriosclerosis,  is  produced  by  the  for- 
mation of  small  areas  of  nodular  infiltrations  in  the  adventitia,  and  gives 
the  vessel  a  nodular  appearance  and  consistency.  It  is  almost  always 
closely  associated  with  inflammatory  changes  in  the  media  and  a  local  pro- 
liferative endarteritis  (Ziegler). 


252 


DISEASES   OF   THE   HEART   AND    AORTA. 


Diffuse  Periarteritis. — The  diffuse  thickening  of  the  adventitia  (periar- 
teritis) is  more  common,  occurring  about  the  arteries  of  the  brain,  about 
the  coronary  arteries  in  myocarditis,  and  in  many  other  organs  in  subacute 
inflammatory  processes.  In  the  radial  and  other  large  arteries  it  seems  to 
be  quite  common.  The  uniformly  thickened  arteries  of  leathery  consistency 
which  are  so  commonly  met  with  in  young  or  middle-aged  persons  who  do 
hard  work  seem  to  be  of  this  type,  though  the  fact  has  not  yet  been  settled 
with  definiteness.  Whether  such  changes  may  be  transitory  or  are  always 
permanent  has  not  been  definitely  settled.  The  boy  of  six  cited  below 
(page  259)  may  perhaps  represent  such  a  case. 


Fig.  154. — Cross  section  of  a  radial  artery  showing  arteriosclerotic  changes  in  the  media.  (Photo- 
micrographs by  Dr.  C.  S.  Bond.)  A.  Cross  section  of  the  entire  artery  (low  power).  B.  Lower  left- 
hand  comer  of  the  same  specimen  (highly  magnified)  showing  destruction  of  the  elastica  interna  and 
thickening  of  the  intima.  C.  Orcein  specimen  showing  destruction  of  the  elastic  fibres  (E)  of  the  media 
with  proliferation  of  white  fibrous  tissue  (F)  and  blood-vessels  (BL).    (Kindness  of  Prof.  W.  Ophiils.) 


Medial  Changes  (Mesarteritis) . — The  rigid  "pipe-stem"  or  "goose- 
neck" radial  arteries  often  met  with  in  very  old  persons  are  formed  by  the 
presence  of  areas  of  degeneration  and  calcification  within  the  tunica  media. 
This  condition  occurring  without  any  changes  in  the  intima  has  been  de- 
scribed in  man  by  Monckeberg,  and  represents  the  type  of  arteriosclerosis 
or  arterionecrosis  produced  experimentalh'-  in  animals  with  bacterial 
toxins,  acids,  adrenalin,  and  alkaloids. 

Calcification. — According  to  Klotz,  Wells,  and  Baldauf,  the  process  of  calcification 
seems  to  go  on  in  the  following  way:  As  a  result  of  the  inflammatory  changes,  the  muscle 
cells  degenerate  and  the  lecithins  become  split  up  into  fatty  acids,  glycerophosphic  acid, 
and  cholin,  causing  the  appearance  of  a  fatty  degeneration.  The  calcium  and  magnesium 
in  the  serum  then  enter  into  combination  with  the  phosphoric  acid  and  are  precipitated  to 


ARTERIOSCLEROSIS. 


253 


form  calcareous  plaques  and  granules  in  the  media.  Klotz  believes  from  histo-chemical 
evidence  that  there  is  intermediate  or  concomitant  formation  of  calcium  soaps,  but  Wells 
and  Baldauf  have  not  found  soaps  on  chemical  analyses.  Baldauf  and  also  Selig  find  that 
most  of  the  calcium  is  in  the  form  of  phosphate  and  sulphate,  little  as  carbonate.  The  ash 
from  arteriosclerotic  plaques  contained  CaO  53.384  per  cent.,  Fe^O^  0.25  per  cent.,  Na^O 
0.72  per  cent.,  K  only  traces,  Rfi,  40.19  per  cent.,  SO3  0.43  per  cent.,  CI  trace,  F  negative, 
CO2  traces  (Selig). 

Klotz  finds  that  the  calcium  is  by  no  means  always  deposited  in  the  patches  of  athe- 
roma, but  exists  also  as  rows  of  fine  granules  between  the  muscle-fibres.     In  this  condi- 
tion it  gives  no  macroscopic  evidence  of  its  presence,  and  merely  causes  a  slight  increase  in 
the  rigidity  of  the  artery.      When  the  necrosis  of  the  arterial 
wall  proceeds  more  slowly,  the  phosphoric  acid  or  glycero- 
phosphoric  acid  derived  from  the  lecithin  is  removed  by  the 
blood-vessels  (capillaries  of  the  vasa  vasorum)  which  enter  the 
diseased  area  of  the  media,  and  the  injured  elastic  tissue  is  v^' 

replaced  by  fibrous  tissue  without  the  deposition  of  calcium.  1i 


Whether  the  calcium  is  deposited  or  not,  the 
area  of  diseased  media  constitutes  a  weak- 
ened portion  of  the  wall  and  is  the  lesion  which 
in  the  large  arteries  is  particularly  responsible  for 
aneurism  formation  (see  also  page  521).  It  has 
been  claimed  by  some  writers  (Heiberg,  Heller, 
and  others)  that  this  lesion  was  confined  to  luetic 
cases,  but  both  clinical  and  experimental  data 
show  that  it  is  due  to  non-luetic  lesions  about 
as  frequently  as  are  any  of  the  other  lesions  of 
arteriosclerosis  (Ophiils). 

Intimal  Thickening. — The  lesion  which  Vir- 
chow,  Thoma,  and  many  writers  have  regarded 
as  the  fundamental  one  in  arteriosclerosis  is  thick- 
ening of  the  intima.  Virchow  believed  that  it  arose 
as  an  inflammatory  hyperplasia  resulting  from  some 
"formative  stimulus"  within  the  blood  stream. 
Thoma  believed  that  this  stimulus  was  the  me- 
chanical factor  of  high  blood-pressure,  and  that 
the  thickening  of  the  intima  represented  a  com- 
pensatory hypertrophy  to  prevent  aneurismal  dila- 
tation; but  Ophiils  has  shown  that,  in  marked 
contrast  to  the  area  of  medial  disease,  there  are  no 
bulgings  of  aortic  wall  at  the  areas  of  intimal 
atheroma,  even  when  the  artery  is  distended  under 
a  pressure  of  160  mm.  Hg. 

The  "formative  stimulus"  is  probably  not  mechanical  but 
chemical,  perhaps  the  same  as  those  which  have  been  shown  experimentally 
to  give  rise  to  arterionecrosis  in  small  animals.  Under  the  influence  of  these 
stimuli  the  intimal  layers  undergo  hyperplasia,  with  increase  of  both  fibrous 
tissue  and  elastic  fibres  (Fig.  156).  Since,  as  Koster  has  shown,  there  are 
no  blood-vessels,  but  only  lymph  spaces  or  lacunar,  the  hyperplasia  soon 
reaches  its  limit,  and  under  the  further  influence  of  the  toxic  agent  the 
cells  at  the  centre  undergo  ''fatty  degeneration"  from  ischajmia.  Such 
areas  present  at  first  a  translucent  appearance  and  are  known  as  areas  of 


Fig.  155. — Arterio.sclerosis 
of  the  descending  aorta,  show- 
ing atheromatous  plaques. 


254 


DISEASES   OF   THE   HEART   AND    AORTA. 


"acute  aortitis."  Later  calcium  salts  are  usually  deposited  (as  described 
above),  and  they  become  converted  into  calcified  plaques  of  atheroma  or 
atheromatous  ulcers.  When  the  process  is  more  chronic  there  is  usually 
a  wandering  in  of  capillaries  from  the  media  after  the  manner  described 
by  Koster,  and  under  the  influence  of  the  improved  nutrition  the  intimal 
hyperplasia  may  go  on  at  an  increased  rate  even  to  the  obliteration  of  the 
lumen  (endarteritis  obliterans).  Thromboangitis  obliterans  will  be  con- 
sidered in  Chapter  IX. 

Unity  of  Arteriosclerotic  Processes.  —  Although  a  large  number  of 
writers  attempt  to  put  each  case  into  one  or  the  other  of  these  groups, 
Ophiils  has  shown,  by  a  careful  complete  study  of  seventy  consecutive 
unselected  cases,  that  such  divisions  are  based  upon  unessential  differences 


Fig.  156.  —  Atheromatous  plaque,   showing  the  changes  in  the  intima.     (Photomicrograph  by  Dr. 

Charles  S.  Bond.) 

and  that,  as  a  matter  of  fact,  any  or  most  of  the  forms  may  arise  in  the 
same  case.  This  division  was  attempted  especially  by  Heiberg,  Heller^ 
and  his  pupils,  who  believed  that  mesarteritis,  particularly  when  it  attacked 
the  first  part  of  the  aorta  and  the  ascending  arch,  was  characteristic  of 
syphilitic  disease.  While  it  is  quite  true  that  syphilis  may  give  rise  to  a 
mesarteritis,  and  occasionally  even  to  the  formation  of  miliary  gummata 
in  the  adventitia,'  nevertheless  these  lesions  are  far  from  characteristic, 
and  very  similar  non-luetic  structures  occur  about  thrombosed  vasa  vasorum. 
Moreover,  Ophiils  was  unable  to  find  any  difference  in  the  distribution  of 
luetic  and  non-luetic  arteriosclerotic  lesions  in  the  seventy  cases  of  his 
series. 

ETIOLOGY. 

The  most  important  etiological  factors  in  the  production  of  arterio- 
sclerosis in  man  are  age,  hard  work,  alcohol,  syphiUs,  and  the  more  acute 

*  Some  writers  claim  to  have  found  the  spirochjjete  paUida  in  these  lesions  by  means 
of  the  rather  questionable  Levaditi's  silver  nitrate  method,  though  Ritter,  Buerger,  and 
many  others  have  failed  in  spite  of  painstaking  search  in  many  cases.  However,  Collins 
and  Sachs,  Longcope,  and  Clough  and  Guthrie  at  the  Johns  Hopkins  Hospital  have  been 
able  to  diagnose  luetic  arteriosclerosis  during  life  by  the  Wassermann  reaction. 


ARTERIOSCLEROSIS.  255 

infectious  diseases,  especially  typhoid  fever.  The  relative  frequency  of 
these  causal  factors,  as  indicated  by  the  palpability  of  the  radial  artery  in 
4000  consecutive  cases  admitted  to  the  Johns  Hopkins  Hospital,  has  been 
made  the  subject  of  a  careful  study  by  Thayer  and  Brush. 

These  observers  found  palpable  arteries  in  the  following  percentage  of  the  patients 
under  fifty  years  who  had  been  subject  to  various  etiological  factors: 

After  scarlatina,  radials  palpable  in 16.4  per  cent. 

No  causal  factor,  radials  palpable  in .  16. 5  per  cent. 

Pneumonia,  radials  palpable  in 17      per  cent- 
Diphtheria,  radials  palpable  in 17      per  cent. 

Malaria,  radials  palpable  in 20      per  cent. 

Typhoid  fever,  radials  palpable  in 26      per  cent. 

Rheumatism,  radials  palpable  in 34      per  cent. 

Alcohol,  radials  palpable  in 46.8  per  cent. 

Hard  work,  radials  palpable  in 57 . 5  per  cent. 

Richard  Cabot  takes  exception  to  these  findings  of  the  high  frequency  of  arteriosclerosis 
after  alcohol,  basing  his  conclusions  upon  autopsies  of  dipsomaniacs  under  fifty  in  whom 
he  says  arteriosclerosis  was  not  present  in  more  than  twenty  per  cent.  His  exceptions  to 
Thayer's  findings  are,  however,  somewhat  against  the  general  consensus  of  opinion,  as  well 
as  against  the  experimental  evidence  of  Aubertin,  who  produced  arteriosclerosis  and  cardiac 
hypertrophy  in  rabbits  by  the  injection  of  alcohol.  On  the  other  hand,  Cabot  is  supported 
by  Fahr,  who  performed  809  autopsies  on  habitual  drunkards  dying  at  the  Harbor  Hospital 
of  Hamburg  and  found  arteriosclerotic  changes  no  more  common  than  in  abstemious  indi- 
viduals, occurring  in  95  cases,  82  of  whom  were  over  40  years  of  age.  Only  7  drunkards  in 
his  series  died  before  40  from  causes  referable  to  arteriosclerosis.  Similar  changes  existed  in 
only  six  other  patients  under  40.  Unlike  Aubertin,  Fahr  was  unable  to  produce  arterio- 
sclerosis in  rabbits  by  administration  of  alcohol  for  over  two  years.  From  this  it  would 
appear  that  the  evil  effects  of  alcohol  have  been  considerably  exaggerated,  at  least  as  far 
as  the  arteries  are  concerned.  It  must  be  borne  in  mind  that  indulgence  in  a  certain 
amount  of  alcohol  is  almost  universal,  especially  in  those  persons  who  do  hard  work,  hence 
it  is  extremely  difficult  to  segregate  these  factors  in  any  large  number  of  cases.  If,  for 
example,  a  patient  has  had  typhoid  fever,  has  used  alcohol,  and  has  done  hard  work,  it  is 
not  logical  to  enter  his  name  into  each  of  the  three  columns,  for  it  is  not  possible  to  deter- 
mine which  of  th3  factors  is  the  most  important. 

Fortunately,  however,  for  the  decision  of  these  doubtful  points,  the  experiments  of 
Pic  and  Bonnamour  (1.  c.)  upon  experimental  adrenalin  arteriosclerosis  have  shown  that 
where  two  factors  are  acting  together,  arteriosclerosis  may  be  produced 
in  conditions  in  which  it  could  not  be  brought  about  by  one  of  them  alone.  Thus,  tuber- 
culosis +  adrenalin  yielded  arteriosclerosis  in  young  rabbits  which  would  not  have  shown 
arteriosclerosis  after  adrenalin  alone,  and  there  is  no  doubt  that  the  same  is  true  in  man. 

Syphilis  is  a  most  important  factor,  especially  in  the  arteriosclerosis 
which  occurs  below  the  age  of  thirty-five.  As  stated  above,  it  was  supposed 
by  Heiberg,  Heller,  and  their  pupils  that  luetic  arteritis  assumed  a  definite 
type,  the  media,  the  adventitia,  and  especially  the  vasa  vasorum  showing 
considerable  small  round-celled  infiltration;  but,  although  it  is  possible 
that  the  media  and  adventitia  are  attacked  more  constantly  than  in  other 
forms,  this  form  is  not  to  be  regarded  as  specific.  The  tendency  to  form 
lesions  above  the  semilunar  valves  and  along  the  ascending  aorta  is  by  no 
means  confined  to  arteritis  of  luetic  origin  (Ophiils),  though  extremely 
frequent  in  the  latter  (Osier,  Collins  and  Sachs,  Longcope).  A  positive 
Wassermann  reaction  is  often  obtained  in  cases  of 
luetic  aortitis  in  which  there  are  no  other  active 
luetic    processes. 


256  DISEASES   OF   THE   HEART   AND    AORTA. 

Lead  poisoning  (especially  chronic  plumbism)  and  gout  are 
important  etiological  factors,  as  is  also  chronic  nephritis.  Overeating 
is  thought  to  play  an  important  role,  especially  when  the  diet  is  rich  in 
meats,  sweetbreads,  livers,  kidneys,  etc., — in  other  words,  in  purin  bodies 
and  in  kreatin.  The  exact  role  of  these  substances  has  not  been  carefully 
studied,  although  Croftan  found  that  long-continued  injection  of  0.5  to 
5.0  mg.  xanthin  into  rabbits  caused  a  rise  of  forty  millimetres  in  blood- 
pressure,  as  well  as  sclerotic  changes  at  least  in  the  renal  arteries.  (He  does 
not  describe  the  condition  of  the  other  arteries.)  From  the  stand-point 
of  both  blood-pressure  and  gaseous  metabolism  it  has  been  shown  that  the 
digestion  of  large  meals  materially  increased  the  work  of  the  body,  pro- 
ducing thereby  an  effect  not  dissimilar  to  that  of  hard  physical  exercise 
(increase  in  pulse-pressure,  increase  in  pulse-rate,  increase  in  CO2  output) 
(effect  of  large  meal,  after  Erlanger  and  Hooker).  It  is  therefore  quite  nat- 
ural that  overeating  should  rank  with  hard  work  as  a  main  cause  of  arte- 
riosclerosis, but  the  exact  extent  of  its  occurrence  is  more  difficult  to  deter- 
mine in  a  large  series  of  cases  than  in  an  individual  case  in  private  practice. 

Lastly,  and  still  more  important  in  the  etiology  of  arteriosclerosis,  are 
age    and   heredity  (Israel) . 

Thus,  Osier  states  that  "entire  famUies  sometimes  show  this  tendency  to  early 
arteriosclerosis,  a  tendency  which  cannot  be  explained  in  any  other  way  than  that  in  the 
make-up  of  the  machine  bad  material  was  used  for  the  tubing."  This  is  especially  true  as 
regards  alcoholism,  as  has  been  shown  in  a  recent  statistical  study  by  Emerson,  who  found 
that  this  factor  was  of  more  importance  than  the  drinking  of  alcohol  by  the  individual 
himself  in  determining  arteriosclerosis  and  longevity,  and  that  an  alcoholic  ancestry  was 
very  frequently  followed  by  a  generation  with  a  tendency  to  early  arteriosclerosis. 

Experimental  Arterionecrosls  In  Animals.  —  A  most  interesting  side 
light  upon  the  genesis  of  arteriosclerosis  has  been  thrown  by  attempts  to 
produce  it  experimentally  in  animals,  especially  in  rabbits  and  guinea- 
pigs.  The  lesions  which  have  been  produced  cannot  be  termed  true  arterio- 
sclerosis like  that  seen  in  man,  but  are  confined  to  the  media  and  adventitia, 
the  intima  always  remaining  clear.  The  reason  for  this  is  not  evident. 
Even  the  possibility  that  in  these  small  animals  the  blood  supply  of  the 
arterial  wall  is  different  from  that  in  man,  and  that  owing  to  this  difference 
lesions  occur  most  readily  in  the  media,  does  not  hold,  since  Ophiils  has 
demonstrated  the  occurrence  of  spontaneous  endarteritis  in  rabbits.  The 
experimental  and  clinical  conditions  seem  to  be  closely  analogous,  but  it 
is  not  possible  to  draw  an  absolute  parallelism  between  them. 

Gilbert  and  Lion  have  been  able  to  produce  arteriosclerosis  experimentally  in  ani- 
mals by  the  injection  of  bacterial  toxins,  and  this  has  been  confirmed  by  Klotz. 
This  fact  is  of  great  importance,  not  only  from  the  stand-point  of  experimental  arterio- 
sclerosis, but  also  because  it  establishes  the  importance  of  bacterial  disease  in  the  etiology 
of  arteriosclerosis  met  with  clinically. 

The  earliest  observation  of  arteriosclerosis  brought  about  by  toxic  action  of  organic 
compounds,  and  one  which  establishes  beyond  doubt  the  deleterious  action  of  tobacco 
upon  the  arteries,  is  that  of  Isaac  Adler,  demonstrating  sclerosis  in  the  smaller  peripheral 
arteries  of  rabbits  as  a  result  of  feeding  them  with  infusions  of  tobacco.  Boveri  confirmed 
these  results  by  giving  infusion  of  tobacco  by  stomach-tube,  and  obtained  atheromatous 
plaques  or  thickening  at  the  base  of  the  aorta  in  ten  out  of  sixteen  rabbits,  while  Baylac 
obtained  sclerosis  in  each  of  eight  rabbits  into  which  tobacco  infusion  was  injected  either 
intravenously  or  subcutaneously.  Jebrowsky  and  later  W.  E.  Lee  have  produced  it  in 
rabbits  made  to  inhale  tobacco  smoke.    From  Baylac's  experiments  it  would  appear  that 


ARTERIOSCLEROSIS.  257 

in  general  the  liability  to  occurrence  bears  some  relation  to  the  channel  by  which  it  enters 
the  body.  This  may  explain  the  very  marked  action  of  tobacco  inhaled  and  entering  the 
heart  directly  from  the  pulmonary  circulation  in  smokers,  as  compared  with  the  somewhat 
milder  effects  of  chewing  tobacco,  under  which  condition  the  nicotine  passes  through  and 
is  perhaps  somewhat  attenuated  in  the  liver  before  entering  the  systemic  circulation, 
and  has  still  to  pass  through  the  vena;  cavae,  right  heart,  and  pulmonary  circulation  before 
reaching  the  coronary  circulation.  In  smoking,  however,  the  nicotine  enters  through 
the  lungs  and  strikes  its  first  blow  at  the  coronary  arteries  and  base  of  the  aorta,  where  the 
elastic  fibres  are  under  the  greatest  tension  and  hence  most  liable  to  degeneration.  It  is, 
therefore,  easy  to  understand  why  smoking  of  heavy  cigars  should  be  one  of  the  most 
potent  factors  in  the  etiology  of  arteriosclerosis  and  coronary  sclerosis. 

An  almost  new  era  in  the  study  of  arteriosclerosis  was,  however,  introduced  by  the 
discovery  of  Josue  that  the  repeated  intravenous  injection  of  adrenalin 
into  rabbits  brought  about  sclerosis  and  calcification  in  the  aorta  within  a  few  weeks. 
This  was  very  soon  confirmed  by  W.  Erb,  Jr.,  who  produced  the  lesions  in  a  large  number 
of  animals,  and  demonstrated  the  considerable  uniformity  with  which  such  lesions  fol- 
lowed the  injections.  Similar  results  have  been  obtained  in  rabbits  by  Fischer  by  the 
intravenous  injection  of  a  very  large  number  of  substances, — h  ydrochloric  acid, 
phosphoric  acid,  lactic  acid,  calcium  phosphate,  chloralainide, 
mercuric  chloride,  trypsin,  diuretin,  and  physiological  salt  solu- 
tion, so  that  the  effect  can  scarcely  be  considered  as  specific  for  adrenahn.' 

On  the  other  hand.  Pic  and  Bonnamour,  as  well  as  Adler  and  Hensel,  have  called 
attention  to  the  fact  that  in  none  of  the  series  of  experiments  published  did  more  than  a 
certain  number  of  the  animals  injected  show  lesions,  and  in  a  very  large  series  the  latter 
showed  that  it  was  practically  impossible  to  produce  arteriosclerosis  in  rabbits  by  these 
poisons  until  they  had  attained  a  certain  age.  After  that  age  arteriosclerosis  occa- 
sionally occurred  spontaneously,  but  could  be  brought  on  with  considerable  frequency  by 
the  injection  of  toxic  substances.  As  stated  above,  Pic  and  Bonnamour  have,  however, 
been  able  to  produce  it  in  young  animals  whose  vitality  was  diminished  by  tuberculosis, 
etc.,  indicating  that  disease  may  be  an  accessory  factor  in  diminishing  the  resistance  of 
the  arteries  to  toxic  influences  which  ordinarily  leave  no  traces.  This  carries  the  clinical 
corollary  that  persons  liable  to  arteriosclerotic  changes  should  particularly  avoid  all  con- 
tributing factors  (alcohol,  tobacco,  hard  work,  etc.)  for  some  time  after  infectious  diseases. 

It  is  quite  remarkable  that  Pearce  and  Baldauf,  as  well  as  other  investigators,  report 
that  they  have  been  able  to  produce  arteriosclerosis,  and  that  Josue  claims  to  have 
produced  permanent  elevation  of  blood-pressure  in  rabbits  by  a  single  injection  of  adren- 
alin, since  Fleisher  and  Loeb  failed  to  do  so  in  a  large  series  of  experiments  in  which  such 
injections  did  produce  severe  myocarditis. 

Mechanism  Producing  Experimental  Arteriosclerosis.  —  The  mechanism  by  which 
arteriosclerosis  is  produced  has  been  the  object  of  considerable  study.  In  the  case  of 
adrenalin  at  least,  Erb  believes  that  a  spasm  of  the  vasa  vasorum  takes 
place,  bringing  about  an  insufficient  blood  supply  to  the  coats  of  the  vessels,  and  thereby 
ischemic  degeneration  of  the  latter,  especially  of  the  tunica  media.  This  view  was  also 
shared  by  Pearce  and  Stanton  and  other  observers,  but  Fleisher  and  Loeb  have  shown 
that  considerable  areas  of  aorta  may  be  kept  ischaemic  by  com- 
pression without  producing  arteriosclerosis.  The  factor  must ,  therefore, 
be  toxic.  It  is  possible  that  in  some  cases  with  high  blood-pressure  actual  rupture  of  the 
weakened  elastic  fibres  takes  place,  which  serves  as  a  centre  for  areas  of  necrosis.  W.  H. 
Harvey  has  shown  that  if  bits  of  excised  aorta  are  filled  with  agar  under  various  pressures 
and  then  transplanted  into  subcutaneous  tissue,  those  under  tension  degen- 
erate more  rapidly.  The  same  is  probably  true  of  the  fibres  within  the  artery. 
Moreover,  Josue  has  shown  that  repeated  injections  of  adrenalin  in  the  rabbit  are  followed 
by  permanent  rise  in  blood-pressure.  An  increase  in  blood-pressure  is  indeed  the  rule  in 
arteriosclerosis,  although,  as  Hasenfeld  has  pointed  out,  it  occurs  only  in  persons  whose  scle- 
rosis involves  the  splanchnic  arteries.  Neither  increase  in  blood-pressure  nor  hypertrophy 
of  the  heart  necessarily  occurs  in  patients  where  these  vessels  are  not  involved.    The 

*  A  summary  of  the  recent  literature  upon  this  point  will  be  found  in  the  papers  of 
Saltykow,  Adler,  and  Benda. 
17 


258 


DISEASES   OF   THE   HEART    AND    AORTA. 


reason  for  this  may  be  that  the  cutting  down  of  the  circulation  of  so  large  an  area  as 
the  splanchnic  region  in  itself  increases  the  resistance  to  blood  flow  and  thereby  raises 
pressure.  There  is  also  no  doubt  that,  besides  the  single  artery  involved  in  the  sclerosis, 
the  latter  is  often  the  result  of  prolonged  vasomotor  spasm  in  the  femoral  artery,  etc. 
On  the  other  hand,  such  spasm  may  be  transitory  and  be  accompanied  by  temporary 
rise  of  blood-pressure  and  sensory  phenomena  which  cause  the  syndromes  described  by 
Pal  as  vasomotor  crises  (see  page  270).  Aubertin,  Vaques,  Wiesel,  and  others  have  found 
hyperplasia  of  the  adrenals  present  in  many  experimental  and  clinical  conditions  in 
which  hypertrophy  of  the  heart  and  high  blood-pressure  are  present.  It  therefore  seems 
quite  possible,  in  the  light  of  these  findings,  that  hypertrophy  of  the  heart  and  arterio- 
sclerosis may  often  be  the  result  of  a  hypersecretion  of  adrenalin,  perhaps 
also  of  some  other  internal  secretions.  Why  this  should  be  associated  with  splanchnic 
arteriosclerosis  is  easy  to  see.  The  latter  condition  tends  to  diminish  the  circulation  through 
the  abdominal  viscera,  and  more  blood  is  thus  shunted  through  the  adrenal  arteries  which 
lie  just  above  the  mesenteries,  thus  bringing  about  an  increase  in  adrenal  secretion. 

It  may  be  added  that  Bayer,  in  Krehl's  clinic,  has  shown  that  some- 
times the  high  blood-pressure  is,  in  part  at  least,  dependent  upon  the 
amount  of  salt  in  the  food,  being  low  on  salt-free  and  high  on  diet  rich  in 
salt,  though  this  is  by  no  means  the  rule. 

DISTRIBUTION    OF    ARTERIOSCLEROTIC    LESIONS. 

As  regards  the  distribution  of  arteriosclerotic  lesions  and  its  relations 
to  etiology,  Harlow  Brooks  has  given  the  following  statistical  summary 
based  upon  notes  of  autopsies  on  400  cases: 


Artery. 

Cases. 

Etiological  factors. 

Aorta 

400 

301 
368 
270 

132 
81 
74 
43 
35 

19 
20 

Alcohol  149,  among  laborers  118,  nephritis  51,  syph- 
ihs  38,  old  age  38.     Males  275,  females  125. 

Visceral  trunks 

Coronary  arteries 

Alcohol  107,  nephritis  35,  syphihs  27,  excessive 
tobacco  9. 

Alcohol  48,  nephritis  21,  syphilis  19. 

Alcohol  43,  nephritis  10,  syphilis  10. 

Alcohol  19,  syi)hilis  9,  senility  9. 

Alcohol  12,  nephritis  8,  syphihs  6,  seniHty  3. 

Alcohol  9,  syphilis  7,  nephritis  4,  endocarditis  2, 
seniHty  2,  tuberculosis  2. 

Syphihs  5,  senility  5,  alcohol  4,  tuberculosis  4, 
nephritis  2. 

Most  of  them  with  alcoholism.  Sclerosis  of  mesen- 
teric, all  cases  with  adiposis. 

Alcohohc  4,  syphilitic  4,  most  of  the  rest  in  primary 
spinal  diseases. 

Brain 

Renal          

Splenic 

Lungs 

Cceliac  axis  and  branches.  . 
Spinal  vessels 

ARTERIOSCLEROSIS    IN    THE    YOUNG. 

Arteriosclerosis  in  infants,  children,  and  young  persons  while  rare  is 
not  extremely  so. 

According  to  Fremont  Smith,  who  has  given  an  excellent  review  of  the  subject, 
congenital  syphihs  is  the  cause  in  about  forty  per  cent,  of  the  cases,  and  diphtheria,  scarlet 
fever,  and  typhoid  fever,  as  well  as  infections  in  the  mother  during  pregnancy,  are  impor- 
tant factors.     The  blood-pressure  is  not  usually  elevated,  often  being  as  low  as  70  mm. 


ARTERIOSCLEROSIS.  259 

Hg.  The  writer  has  seen  one  case  of  a  boy  aged  six  suffering  from  acute  nephritis,  com- 
plicated by  lobar  pneumonia,  large  bacillus  coli  abscess  of  the  buttocks,  cystitis  caused  by 
the  same  germ,  who  in  spite  of  continuously  low  blood-pressure  developed  tortuous  and 
apparently  thickened  temporal  and  thickened  radial  arteries.  After  a  few  months  these 
arteries  were  no  longer  palpable.  It  is  possible  that  these  changes  may  have  been  merely 
mononuclear  infiltration  about  the  vessels  of  the  adventitia. 

CLINICAL    MANIFESTATIONS    OF    ARTERIOSCLEROSIS. 

Clinically,  the  symptoms  due  to  arteriosclerosis  usually  express 
themselves  in  several  groups  dependent  upon  the  arteries  most  affected. 

(1)  Cardiac,  associated  with  myocarditis  and  coronary  sclerosis; 
often  with  renal  symptoms  (see  Chapter  IX).  As  shown  by  Fleisher  and 
Loeb,  the  myocarditis  may  be  produced  by  the  same  cause  and  may  be 
more  severe  than  the  arteriosclerosis  itself. 

(2)  Simple  coronary  sclerosis,  paroxysmal  dyspnoea,  angina 
pectoris,  Adams-Stokes  syndrome,  paroxysmal  tachycardia,  sudden  death. 

(3)  Cerebral   symptoms. 

(4)  Aneurism. 

(5)  Intermittent  claudication. 

(6)  Vasomotor  crises  (Pal) : 

(a)  Abdominal  pain  from  vasoconstriction; 

(6)   Raynaud's  disease; 

(c)  Pain  down  arms  and  legs. 
The  clinical  characteristics  of  the  cardiac  and  renal  cases  have  been 
discussed  in  Chapter  IX  under  the  head  of  the  myocarditis  which 
invariably  accompanies  them.  They  may  be  briefly  summarized  as 
shortness  of  breath,  especially  on  exertion,  often  asthmatic  or 
paroxysmal  in  character;  palpitation;  weakness;  occasionally  a 
considerable  degree  of  nervousness,  loss  of  memory,  and  insomnia. 
In  advanced  cases  with  some  sclerosis  of  cerebral  arteries  there  may  be  more 
or  less  transient  irrationality,  especially  at  night  or  on  awakening. 
There  may  be  pains  over  the  precordium,  in  the  shoulders,  or  down 
the  arms,  or  in  the  abdomen  or  legs,  which  may  be  definitely  associated 
with  periods  of  high  blood-pressure  (the  vasomotor  crises  of  Pal) ;  there 
may  be  sudden  pain  and  sudden  paralysis  of  a  leg,  disap- 
pearing on  rest,  reappearing  after  a  few  steps  are  taken  (intermittent 
claudication,  Charcot,  Erb) ;  or  there  may  be  severe  precordial  pain  with 
a  feeling  of  weight  and  constriction  over  the  sternum  and  an  utterable 
fear  of  impending  death  (angina  pectoris).  On  the  other  hand,  the  hand 
or  foot  may  become  cold  or  numb,  the  pulsation  disappear  from 
the  arteries,  intense  pain  set  in  (Raynaud's  disease),  or  finally  be  followed 
by  gangrene  (thromboangitis  obliterans).  Still  further  the  patient  may 
suffer  from  all  the  signs  and  symptoms  of  aneurism. 

On  physical  examination  the  radial  arteries  may  or  may  not  be 
found  to  be  thickened  or  be  a  de  d  (atheromatous),  dependent  partly 
upon  the  distribution  of  the  sclerosis,  since  the  radial  artery  may  be  spared. 
Some  writers  state,  however,  that  in  men  who  do  hard  manual  labor  the 
radial  arteries  are  the  first  attacked,  while  in  those  who  lead  a  sedentary 
life  sclerosis  may  appear  very  early  about  the  base  of  the  aorta,  and  the 
radial,  nevertheless,  may  be  perfectly  normal. 


260 


DISEASES   OF   THE    HEART    AND    AORTA. 


The  artery  in  which  the  sclerosis  is  next  most  readily  observed  is  the 
temporal,  which  usually  stands  out  like  a  cord  or  is  very  tortuous,  and  when 
pressed  against  the  bone  feels  thickened  and  leathery.  This  tortuosity 
may  also  be  present  in  the  brachials  and  even  in  the  abdominal  aorta,  and 
is  probably  brought  about  by  the  stress  of  the  arterial  tension  exerted  upon 
the  walls,  which  are  in  some  places  weaker  and  less  elastic  than  in  others; 
so  that  we  have  a  force  (blood-pressure)  which  is  exerted  equally  on  all 
sides  against  walls  which  interpose  a  greater  resistance  on  one  side  than  on 
the  other,  hence  the  curvature  results.  As  might  be  expected,  the  tortu- 
ousness  is  therefore  greater  when  the  disturbing 
force  is  high  (high  blood-pressure)  and  less  when 
it  is  low,  as  shown  in  the  figure  (Fig.  157). 

Other  superficial  arteries  which  may  be  felt 
are  the  brachials,  axillaries,  facials,  popliteals,  and 
dorsalis  pedis. 

Changes  in  the  Retinal  Vessels.  —  Hirschberg 
in  1882  called  attention  to  the  fact  that  changes 
in  the  retinal  vessels  constitute  an  early  sign  of 
arteriosclerosis,  and  later  demonstrated  that  this 
change  was  normal  in  old  persons  and  usuallj'  began 
in  the  fifth  decade.  Friedenwald  and  Preston  exam- 
ined twenty-three  persons  suffering  from  general 
arteriosclerosis,  and  found  only  seven  normal  reti- 
nas among  them. 

De  Schweinitz  gives  the  following  criteria  for  sclerosis  of 
the  retinal  vessels: 

(1)  Suggestive  Signs. — Uneven  caliber  and  undue  tortu- 
ousness  of  the  retinal  arteries  (corkscrew  form),  increased  dis- 
tinctness of  the  central  light  streak,  an  unusually  light  color  of 
the  artery,  and  alterations  in  the  course  and  caliber  of  the  veins. 

(2)  Pathognomonic  Signs. — Changes  in  size  and  breadth 
of  the  arteries,  loss  of  translucency,  lesions  in  the  arterial  walls 
consisting  of  white  stripes  in  the  form  of  perivasculitis,  inden- 
tation of  the  veins  by  the  stiffened  arteries,  tortuousness  of 

veins  and  white  stripes  or  varicosities  along  their  courses,  oedema  of  the  retina  in  the 
form  of  gray  opacity  around  the  disk  or  following  the  course  of  the  vessels,  hemorrhages 
as  linear  extravasations  or  roimdish  infiltrations.  Sometimes  very  sudden  changes  in 
the  caliber  of  the  retinal  arteries  may  be  seen  accompanjnng  vasomotor  crises. 


Fig.  157. — Tortuou-s  radial 
artery.  (After  Pal.)  Solid  line, 
course  of  the  radial  artery  at 
200  mm.  Hg  blood-pres.sure. 
Broken  line,  course  of  the  ar- 
tery at  95  mm.  blood-pressure, 
after  amyl  nitrite. 


X-ray  Examination. — Absolute  proof  of  arteriosclerosis  is  also  given 
by  the  X-ray,  by  which  calcified  plaques  along  the  course  of  deepl}'  situated 
arteries  (popliteals,  femorals,  abdominal  aorta,  etc.)  may  be  discerned  as 
distinct  shadows  ranged  along  the  course  of  the  arterj'.  These  may  be 
brought  out  more  distinctly  by  using  two  stereoscopic  pictures  instead  of 
one.  Unfortunately,  it  has  not  been  possible  to  discern  sclerosis  of  the 
coronary  arteries  in  this  waj'. 

Sclerosis  of  the  Abdominal  Aorta. — Arteriosclerosis  of  the  abdominal 
aorta  and  splanchnic  vessels  is  very  common,  as  has  been  shown  by  Hasen- 
feld.  Bond,  Brooks,  Ortner,  and  Gilbride.  In  fact,  it  may  almost  be  diagnosed 
with  certainty  when  the  blood-pressure  is  elevated.  Occasionally  the  course 
of  the  abdominal  aorta  may  be  felt  to  be  tortuous.    Sclerosis  of  the  abdom- 


E  F 

Fig.  158. — Retinal  changes  in  arteriosclerosis.  A,  Normal  fundus.  B  to  F,  successive  changes 
occurring  in  arteriosclerosis,  including  pallid  arteries  (B),  later  assuming  a  silver-wire  appearance  (C); 
indented  veins  (B,  C),  afterward  showing  ampulliform  enlargements  (D,  E);  corkscrew  capillaries  (C,  D); 
corkscrew  arteries  and  veins  (D,  E);  perivasculitis  (C,  D);  sclerosis  of  vessels  (F);  oedema  of  disk 
(B,  C,  D,  E).  hemorrhages  (C  F).— D.     (After  de  Schweinitz.) 


ARTERIOSCLEROSIS. 


261 


inal  vessels  is  not  infrequently  accompanied  by  crises  of  severe  abdominal 
pain  not  unlike  those  of  tabes  (abdominal  vasomotor  crises),  but  these  may 
also  be  present  from  simple  pulsation  of  the  abdominal  aorta  when  tugging 
upon  loose  peritoneal  moorings.  Sclerosis  of  the  pancreatic  artery  is  often 
accompanied  by  diabetes  mellitus. 

BLOOD-PRESSURE    AND    PULSE. 

In  arteriosclerosis  the  mechanical  factors  affecting  blood-pressure 
tend  to  approach  those  in  a  system  of  rigid  tubes, — a  high  pressure  through- 
out systole,  a  low  pressure  in  diastole.  In  such  a  system  we  should  have, 
as  a  rule,  a  greater  difference  between  pressure  in  systole  and  in  diastole 
than  when  the  normal  elasticity  tends  to  keep  up  the  diastolic  pressure, 
so  that  the  pulse-pressure  is  often  more  than  50  to  60  mm.  rather  than  being 
nearer  30  or  40  mm.  as  in  the  normal  individual. 


Fig.  159. — Effect  of  arteriosclerosis  upon  the  circulation.  I,  normal.  II,  arteriosclerosis,  with 
high  peripheral  resistance  and  anacrotic  form  of  pulse  wave;  the  arrow  points  to  a  rise  in  maximal  and 
minimal  pressiue  and  increased  pulse-pressure.  Ill,  arteriosclerosis  with  low  peripheral  resistance, 
showing  low  blood-pressure  and  increased  pulse-pressure  and  collapsing  pulse. 

Pulse. — The  pulse  may  assume  any  form  whatever,  from  collapsing 
and  almost  water-hammer  in  character  to  an  anacrotic  plateau,  or  even 
in  rare  cases  to  a  pulsus  tardus.  These  depend  upon  the  relation  between 
strength  and  size  of  beat  and  outflow  through  the  arterioles.  Thus,  if  the 
peripheral  arteries  or  any  large  areas  of  blood-channels  are  dilated  and 
lacking  in  elasticity,  there  will  be  a  momentary  rise  in  pressure  at  the  begin- 
ning until  the  pressure  w^ave  is  transmitted  from  the  aorta  to  the  periphery. 
When  it  reaches  this  point  there  is  a  sudden  outflow  through  those  vessels 
and  a  sudden  fall  or  collapse,  which  is  greater  than  it  would  be  in  a  more 
elastic  system  (see  Fig.  159).  On  the  other  hand,  if  the  peripheral  outflow 
is  small,  the  pressure  in  the  non-elastic  system  quickly  rises  higher  than 
in  an  elastic  system  and  remains  so  throughout  systole,  forming  a  systolic 
plateau  (anacrotic  pulse)  with  a  large  rapid  rise  and  plateau  reaching  to 
the  end  of  systole,  then  a  gradual  fall  during  diastole.  The  pulse  form 
accordingly  gives  us  the  information  in  arteriosclerosis  as  in  other  condi- 
tions (see  page  44),  —  namely,  indicates  low  peripheral  resistance  when 
it  is  collapsing  and  high  peripheral  resistance  when  it  is  anacrotic  or  sus- 


262 


DISEASES   OF   THE   HEART    AND    AORTA. 


tained.  The  pulse  may  either  be  quite  large  or  very  small,  dependent  upon 
the  degree  either  of  vasoconstriction  or  of  endarteritis.  Its  character  may 
be  very  variable;  it  may  be  quite  quick  and  collapsing,  corresponding  to  a 
general  rigidity  of  the  whole  vascular  system,  or  the  vessel  may  fill  rapidly, 
remain  well  sustained  with  long  systolic  plateau,  and  may  then  decline 
either  rapidly  or  slowly.  However,  the  lumen  of  the  radial  artery  may 
have  decreased  so  much  from  an  endarteritis  that  the  filling  of  the  artery 
is  slow  and  the  up-stroke  on  the  pulse-tracing  very  obhque,  just  as  would 
be  typical  of  aortic  stenosis.  This  is  not  extremely  common,  and  the  very 
quick  up-stroke  is  the  form  most  frequently  seen.  On  the  other  hand,  in 
rarer  cases  when,  as  Romberg  and  also  Hasenfeld  have  pointed  out,  the 
splanchnic  vessels  are  not  involved,  the  maximal  blood-pressure  may  be 
quite  normal  (110-120  mm.)  and  the  minimal  also  (90  mm.). 

BIood=pressure.  —  The  blood-pressure  is  often  high.  Thayer  found 
in  his  studies  of  post-typhoid  arteriosclerosis  that  the  maximal  blood- 
pressure  was  usually  20-30  mm.  higher  than  for  normal  individuals  of 
corresponding  age. 

Romberg  and  Sawada,  on  the  other  hand,  found  that  this  occurred  in  only 
12.5  per  cent,  of  all  arteriosclerotics,  while  Groedel  found  hypertension  in  only  37 
per  cent,  of  446  cases  of  arteriosclerosis  free  from  chronic  nephritis.  Dunin  found 
similar  results.  Israel,  however,  found  hypertension — over  140  mm.  Hg  or  180  cm. 
HjO  (v.  Recklinghausen  apparatus) —  in  64.4  per  cent,  of  4.5  cases  of  arteriosclerosis.  The 
minimal  pressure  was  also  increased,  but  less  than  the  maximal.  Israel  gives  the 
following  average  figures: 


Normal — 

cm.  H2O 

mm.  Hg 

Arteriosclerosis — 

cm.  HjO 

mm.  Hg 

Average  increase — 

mm.  Hg 


Max. 

Min. 

Mean. 

170 

110 

140 

125 

81 

103 

240 

140 

190 

177 

103 

140 

52 

23 

37 

Pulse-pressure 
(amplitude). 


60 
44 

100 
74 

30 


Israel's  figures  accord  well  with  the  writer's  experience  (using  the  Erlanger  ap- 
paratus). The  highest  of  these  blood-pressures  are  seen  in  cases  with  chronic  nephritis 
(Israel,  Janeway,  Horner).  The  writer  has  often  found  a  maximal  pressure  of  220  mm. 
Hg  with  a  minimal  of  160,  though  usually  in  association  with  nephritis. 

As  has  been  seen  under  cardiac  overstrain,  the  presence  of  arterio- 
sclerosis has  a  marked  effect  in  impairing  the  bodily  strength  and  the  ability 
to  withstand  strain.  The  diminution  in  arterial  bed  increases  the  total 
work  of  the  heart,  and  the  patches  of  arterial  fibrosis  prevent  the  arteries 
from  dilating  under  functional  activity.  On  the  other  hand,  the  loss  of 
arterial  elasticity  removes  a  factor  which  tends  to  propel  the  blood  during 
diastole  and  thus  to  maintain  the  blood  flow  at  the  least  expenditure  of 
energy  by  the  heart.  As  a  result  of  this  factor,  the  heart  is  compelled  to 
increase  its  systolic  output  (increased  pulse-pressure)  under  normal  condi- 


ARTERIOSCLEROSIS.  263 

tions  and  hence  has  little  ability  for  further  increase  in  reserve.  Muscular 
effort  therefore  gives  rise  to  signs  of  greater  strain  than  in  normal  individ- 
uals, greater  increase  in  blood-pressure,  and  greater  fatigue. 

The  intensity  of  vasomotor  reactions  varies  considerably  in  different 
cases  of  arteriosclerosis.  In  some  cases,  as  Romberg  has  shown,  the  vaso- 
motor reaction  of  the  arm  vessels  to  cold  may  entirely  disappear;  while  in 
others  (vasomotor  crises)  the  reactions  are  so  intense  as  to  produce  ischsemia 
of  the  parts. 

The  Second  Aortic  Sound. — Corresponding  to  the  high  blood-pressure 
there  is  also  accentuation  of  the  second  aortic  sound,  which  on  the  one  hand 
ma}^  be  due  to  the  heightened  blood-pressure  and  the  greater  tension  of  the 
aortic  valves,  or,  on  the  other,  to  the  thickening  and  partial  calcification 
of  the  valves  themselves,  w^hich  gives  rise  to  a  louder  sound  than  usual 
when  the  valves  strike  together,  even  under  the  usual  pressure.  A  marked 
accentuation  of  the  aortic  second  sound  therefore  always  leads  to  the 
suspicion  of  arteriosclerosis,  even  in  the  absence  of  thickening  in  the  walls 
of  the  superficial  vessels.  However,  it  is  not  pathognomonic,  since  it  may 
ofteii  be  heard  in  cases  where  no  special  sclerosis  is  present,  especially  at 
times  when  the  heart  is  acting  strongly  and  probably  giving  forth  a  larger 
output  into  the  aorta  at  each  systole,  as  in  typhoids  with  dicrotic  pulse 
or  in  perfectly  healthy  young  persons  during  attacks  of  palpitation.  In 
such  cases  the  accentuation  of  the  second  sound  is  transitory. 

BLOOD    COUNT    IN    ARTERIOSCLEROSIS. 

The  blood  count  may  vary  considerably,  first  on  account  of  the  great 
variety  of  diseases  associated  with  arteriosclerosis,  and  secondly,  because 
the  latter  is  sometimes  accompanied  by  polycythsemia  or  erythremia. 

There  are  no  blood  changes  which  in  themselves  can  be  said  to  be  defi- 
nitely associated  with  arteriosclerosis. 

AORTIC    SCLEROSIS. 

When  the  aortitis  near  the  base  of  the  aorta  is  marked,  and  especially 
if  calcified  plaques  are  present,  the  first  sound  as  well  as  the  second  may  be 
changed  and  may  be  accompanied  by  a  loud  murmur  which  is  usually  trans- 
mitted to  the  carotid  and  brachial  arteries,  resembling  that  heard  in  aortic 
stenosis  but  less  intense.  Since  the  condition  is  much  more  common  than 
the  latter,  this  murmur  is  also  more  commonly  due  to  this  cause,  but  in 
the  absence  of  the  characteristic  pulse  it  is  quite  indistinguishable  from 
that  of  aortic  stenosis,  for  both  arise  at  the  same  site  at  the  same  time  and 
are  transmitted  in  the  same  way.  The  murmur  is  often  accompanied  by 
a  marked  thrill  having  the  same  distribution  and  is  followed  by  a  distinct 
diastolic  shock. 

As  regards  sclerosis  of  the  aorta  alone,  Bittorf  ha3  found  that  it  frequently  occurs  at 
an  average  age  of  fifty-five  (forty-five  in  syphilitics)  as  a  result  of  the  usual  factors;  some- 
times a  single  trauma  to  the  chest  may  seem  to  be  the  important  moment  in  the  etiology. 
It  is  especially  common  in  syphilitics  and  fat  persons,  and  is  frequently  associated  with 
pale,  ashy-gray  color,  very  high  blood-pressure  (170  to  220  mm.),  occasionally  difference 
in  size  of  the  pupils,  pains  over  the  chest  and  down  the  arms,  oedema  over  the  sternum, 


264  DISEASES   OF   THE   HEART    AND    AORTA. 

unilateral  dilatation  of  veins  in  second  and  third  interspaces,  ringing  aortic  second  sound 
without  diastoHc  murmur,  hypertrophy  of  the  heart,  often  pulsus  celer,  rarely  pulsus 
tardus  or  pulsus  paradoxus.  Cardiac  pain  may  be  present,  often  felt  just  after  percus- 
sion, and  described  as  something  boring  through  the  sternum,  sometimes  with  a  feeling  of 
constriction,  sometimes  radiating  to  the  arms  and  neck.  Occasionally  spells  of  weakness 
in  the  arms  may  be  felt  not  unlike  intermittent  claudication. 

The  differential  diagnosis  from  aortic  stenosis  is  made  by  the  gradual 
up-stroke  on  the  pulse  tracing  in  the  latter  case,  as  contrasted  with  the  sudden  up-stroke 
and  plateau  in  the  former;  from  aortic  insufficiency  by  the  diastolic  murmur  and  high 
pulse-pressure;  from  aneurism  by  the  percussion  and  fluoroscopic  findings.  Nevertheless, 
it  must  be  admitted  that  many  doubtful  cases  arise. 


SCLEROSIS    OF    THE    PULMONARY    ARTERY. 

Primary  sclerosis  of  the  pulmonary  artery  is  not  extremely  rare,  but  is  difficult  or 
impossible  to  diagnose  with  certainty;  but  the  presence  of  very  loud  sounds  in  the  pul- 
monic area  or  of  a  rough  systolic  murmur  heard  loudest  at  the  pulmonic  and 
transmitted  upward  towards  the  left  clavicle  arouses  the  suspicion  of  a  pulmonary 
8clerosi.s,  especially  if  signs  of  congenital  lesion  are  absent  and  the  murmur  is  not  heard 
over  the  carotid.  However,  sclerosis  of  the  pulmonary  artery  is  often  secondary  to 
mitral  stenosis  and  emphysema. 

C.\SE  OF  Primary  Pulmonary  Sclerosis. 

Romberg  reports  the  case  of  a  man,  aged  24,  who  had  had  no  infectious  diseases 
except  measles  as  a  child  and  a  recent  slight  muscular  rheumatism,  three  months  after 
which  he  began  to  have  gradually  increasing  shortness  of  breath,  epigastric 
pressure,  occasional  headaches  and  giddiness,  and  his  color  became  very  blue.  On  ex- 
amination he  showed  marked  cyanosis  over  the  face,  body,  and  limbs. 
There  was  a  pulsation  due  to  the  right  ventricle  in  the  fourth  interspace  4  cm.  inside  the 
mammillary  line  and  thence  inward  to  the  sternum,  also  a  smaller  pulsation  (left  ventricle) 
in  the  fifth  interspace  mammillary  line,  cardiac  dulness  7  cm.  to  right,  15  cm.  to  left.  Both 
pulmonic  sounds  were  louder  than  the  aortic.  Pulse  small,  regular,  116.  Liver  enlarged; 
spleen  enlarged.    No  oedema;  no  swelling  of  vessels  of  neck. 

Probable  diagnosis  (Curschmann) ,  congenital  heart  lesion.  Patient  gradually  became 
worse;   digitalis  was  without  effect.    Died  one  month  after  admission. 

Autopsy  showed  enlarged  heart;  right  ventricle  hypertrophied  and 
forms  the  entire  apex,  and  the  con  us  arteriosus  and  right  auricle  are  espe- 
cially hypertrophied.  All  the  valves  intact  and  normal;  aorta  free  from  sclerosis, 
but  unusually  small.  Ductus  arteriosus  closed.  Tremendous  sclerosis  and 
atheroma  of   the   pulmonary   artery   and  all  its  branches.' 

The  murmur  may  be  distinguished  over  the  abdominal  aorta  and  the 
femoral  artery,  though  the  thrill  is  rarely  transmitted  so  far.  There  is  no 
Duroziez  double  murmur  unless  aortic  insufficiency  is  also  present. 

Sanders  has  recently  collected  similar  cases  from  the  literature. 

TREATMENT. 

The  general  treatment  of  arteriosclerosis  is  mainly  prophylactic, 
hygienic,  and  dietetic,  and  actual  specific  treatment  is  of.  far  less  value. 

Diet. — Carefully  selected  diet  is  a  most  important  factor,  restriction 
being  in  both  quality  and  quantity.  The  general  diet  given  in 
heart  cases  (see  page  167)  is  of  great  benefit  here,  or  equivalent  diets  with 

'  Notes  of  a  case  of  pulmonary  arteriosclerosis  (O.  A.  K.)  secondary  to  mitral  stenosis 
are  given  on  p.  354. 


ARTERIOSCLEROSIS.  265 

this  as  a  basis.  However,  in  simple  arteriosclerosis  the  quantity  taken  at 
a  time  need  not  be  so  greatly  restricted;  but  the  total  quantity  in  twenty- 
four  hours  should  not  exceed  twenty-five  hundred  calories,  and  should 
always  be  near  the  lower  level  for  proteids,  and  as  free  as  possible  of  purin 
bodies  (nitrogenous  extractives  such  as  are  found  in  meat),  creatinin,  etc., 
and  also  of  salt.  The  more  recent  studies  quoted  above  seem  to  indicate 
that  excess  in  salt  is  almost  as  injurious  as  are  excesses  in  alcohol,  and  that 
the  salt  mackerel  of  Boston  is  as  dangerous  as  the  beer  of  Milwaukee.  For 
the  sclerotic  danger  probably  lurks  in  the  Smithfield  ham  or  the  cold  smoked 
tongue  as  well  as  in  the  Baltimore  rye  or  the  Martini  cocktail  (Beyer,  Barie, 
Hadfield).  The  patient's  safety  lies  in  milk,  eggs,  potatoes,  bread,  other 
carbohydrates,  butter,  and  the  simpler  fruits. 

Restriction  of  Liquids.  —  On  the  other  hand,  the  liquid  intake  also 
should  not  be  excessive,  since  drinking  large  amounts  either  of  water  or 
of  beer  seems  to  favor  sclerosis  (Krehl),  but  the  amount  ingested  should 
remain  in  the  vicinity  of  fifteen  hundred  cubic  centimetres  a  day,  some 
persons  thriving  best  at  five  hundred  cubic  centimetres  above,  some  at 
five  hundred  cubic  centimetres  below  this  level. 

Tobacco  and  alcohol  should  be  dispensed  with  entirely  if  possible ; 
if  the  patient  insists  on  taking  small  quantities,  one  or  two  light  dry  cigars, 
as  thin  as  possible  (Lee),  or  "stogies,"  a  day  are  perhaps  the  mildest  that 
one  may  prescribe.  Cigarette  smoke  is  usually  inhaled  and  pipes  are  very 
heavy.    Thick  Havana  cigars  should  be  entirely  prohibited.  < 

As  to  alcohol,  if  the  patient  insists  upon  taking  a  small  quantity, 
this  should  be  limited  to  an  occasional  glass  of  claret  or  white  wine,  or 
perhaps  a  single  glass  of  beer  at  rare  intervals.  The  latter  in  large  quan- 
tities is  especially  undesirable,  both  on  account  of  the  large  amounts  of 
liquid  taken  and  because  it  contains  both  alcohol  and  proteid  and  purin 
substances  extracted  from  the  yeast.  Gin  is  perhaps  more  dangerous 
than  whiskey. 

Coffee  and  tea  should  be  taken  in  only  small  quantities,  since 
the  vasoconstrictor  action  of  the  caffeine  favors  the  onset  of  spasmodic 
vasoconstriction  (vasomotor  crises),  and,  on  the  other  hand,  the  increase  of 
blood-pressure  itself  brought  on  by  caffeine  is  damaging  to  the  arteries. 
However,  it  must  be  stated  that,  in  contrast  to  nicotine,  lead,  adrenalin, 
etc.,  injections  of  caffeine  into  animals  have  thus  far  failed  to  bring  on 
arteriosclerosis  and  that  perhaps  the  deleterious  effect  of  caffeine  may  be 
overestimated. 

Hydrotherapy. — Systematic  hydrotherapy  is  of  considerable  value  in 
arteriosclerosis,  especially  the  use  of  warm  baths,  warm  douches 
(Brieger),  or  alternating  warm  and  cold  douches  (Riley)  applied  both  locally 
and  generally.  They  owe  their  efficacy  to  the  vasodilatation  which  they 
bring  about,  and  hence  must  be  classed  in  effect  with  the  drugs  of  the  nitrite 
group.  In  most  cases  the  effect  of  a  good  warm  douche  or  warm  bath  is 
more  marked  and  more  lasting  than  that  of  any  of  these  drugs,  and  it  is 
further  devoid  of  that  certain  residuum  of  deleterious  effect  which  all 
drugs  leave  behind  them.  So  that,  while  one  cannot  agree  with  Brieger 
that  arteriosclerosis  can  be  entirely  cured  symptomatically  by  proper 
hydrotherapy,  nevertheless  warm   baths    and   warm   showers 


266  DISEASES   OF   THE   HEART   AND    AORTA. 

once  or  twice  a  day  should  be  an  indispensable  part 
of  the  treatment  of  every  arteriosclerotic.  Cold  baths 
should  be  avoided,  since  they  precipitate  vasomotor  reactions,  which  in 
the  arteriosclerotic  may  amount  to  vasoconstrictor  spasm. 

Drugs.  —  Potassium  Iodide.  —  As  to  drugs,  universal  experience  points 
to  the  efficacy  of  potassium  iodide  in  doses  ascending  from  0.3 
Gm.  (gr.  v)  t.i.d.,  p.c,  to  as  high  as  4  Gm.  (5i) ;  some  clinicians  favor- 
ing the  smaller,  some  the  larger  doses.  In  the  writer's  experience  doses 
under  1  Gm.  (gr.  xv)  seem  to  have  some  effect  in  alleviating  symptoms; 
and  when  there  is  a  suspicion  of  lues  the  dose  should  be  increased  still 
further.  (The  therapeutic  action  and  its  limitations  are  discussed  in 
Chapter  V.) 

It  has  been  attempted  to  settle  the  question  experimentally  by  deter- 
mining the  effect  of  potassium  iodide  upon  the  course  of  adrenalin  atheroma 
in  rabbits.  Koranyi,  Boveri,  and  Cummins  and  Stout,  who  were  the  first 
to  undertake  these  investigations,  all  reported  that  potassium  iodide  or 
iodipin,  when  injected  during  the  time  that  adrenalin  was  being  injected, 
inhibited  the  production  of  atheroma.  However,  it  must  be  borne  in  mind 
that  Biland,  Loeb  and  Githens,  Adler  and  Hensel  found  that  large  doses 
of  potassium  iodide  seemed  to  increase  rather  than  inhibit  the  atheromatous 
changes.  It  is  at  present  impossible  to  tell  exactly  what  quantity  repre- 
sents the  optimum  dose  for  human  beings,  and  whether  therapeutic  doses 
ever  reach  the  stage  of  harmfulness. 

While  sclerosis  of  the  pulmonary  artery  secondary  to  the  pulmonary 
stasis  of  mitral  stenosis  is  relatively  common,  primary  sclerosis  of  this 
artery  is  rather  rare. 

Nitrites. — Next  to  the  iodides  in  general  use  is  the  group  of  nitrites, — 
amyl  nitrite,  nitroglycerin,  sodium  nitrite,  erythrol  tetranitrate.  These 
drugs  are  of  value  for  symptomatic  treatment,  to  relieve  pain  or  discomfort 
for  the  time  being,  but  they  exercise  no  inhibitory  influences  upon  the  prog- 
ress of  the  arteriosclerosis,  as  has  been  shown  for  adrenalin  arteriosclerosis. 
On  the  other  hand,  their  effect  upon  the  symptoms  due  to  arteriosclerosis, 
the  pain  of  intermittent  claudication,  of  angina  pectoris,  of  the  abdominal 
and  peripheral  vascular  crises,  is  most  remarkable,  and  in  this  regard  they 
are  invaluable  (Lauder  Brunton).  However,  in  their  administration  it 
must  be  borne  in  mind  that  persons  with  arteriosclerosis  seem  to  have 
considerable  tolerance  for  nitrites  (page  188),  and  to  bring  about  vasodila- 
tation and  fall  in  blood-pressure  much  larger  doses  must  be  given  than  is 
necessary  to  produce  the  effect  in  normal  individuals.  Accordingly,  as 
indicated  in  Chapter  V,  the  drug  should  be  administered  in  increasing 
doses  until  the  physiological  effect  (flushing,  throbbing  in  head,  ringing 
of  the  ears)  is  obtained,  and  then  continued  in  a  dose  just  a  little  smaller 
than  this.  One  need  not  be  surprised,  however,  to  find  that  this  dose  for 
a  person  with  arteriosclerosis,  particularly  a  colored  person,  may  be  ten 
or  even  twenty  times  the  average  dose  for  a  normal  individual.  When 
such  is  the  case  the  blood-pressure  is  probably  a  beneficial  compensatory 
phenomenon,  and  the  nitrites  should  be  discontinued. 

In  the  chronic  hypertension  of  arteriosclerosis  venesection  is 
not  only  useless  but  often  harmful. 


ARTERIOSCLEROSIS.  267 

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of  Arteriosclerosis,  J.  Am.  M.  Asso.,  Chicago,  1891,  xvi,  623. 
De  Schweinitz,  G.:  Intra-ocular  Angiosclerosis,  and  its  Prognostic  and  Diagnostic  Sig- 
nificance, Internat.  Clinics,  Phila.,  1907,  17th  Ser.,  vol.  i,  177. 
Romberg  and  Hasenfeld.     Quoted  on  p.  213. 
Thayer,  W.  S.:  On  the  Late  Effects  of  Typhoid  Fever  on  the  Heart  and  Vessels,  Am. 

J.  M.  Sc,  Phila.  and  N.  York,  1904,  cxxvii,  391. 
Romberg,  E.:  Ueber  Arteriosklerose.  Verh.  d.  Kong.  f.  innere  Med.,  Wiesb.,  1904,  xxi,  60. 
Sawada:  Blutdruckmessung  bei  Arteriosklerose,  Deutsch.  med.  Wchnschr.,  1904,  xxx,  425. 
Groedel:  Ueber  den  Wert  der  Blutdruckmessung  fiir  die  Behandlung  der  Arteriosklerose, 

Verhandl.  d.  Kong.  f.  inn.  Med.,  Wiesb.,  1904,  xxi,  113. 
Israel,   A.:     Klinische  Beobachtungen  ueber  das  Symptom  der  Hypertension,  Samml. 

klin.  Vertr.,  Leipz.,  1907.     Innere  Med.,  No.  135-136. 
Janeway  and  Horner.     Quoted  on  p.  35. 
Bittorf,   A.:     Zur  Symptomatologie  der  Aortensklerose,  Deutsch.   Arch.  f.   klin.   Med., 

Leipz.,  1904,  Ixxxi,  65. 
Romberg,  E.:    Ueber   Sklerose  der  Lungenarterie,  Deutsch.  Arch.  f.  klin.  Med.,  Leipz., 

1891,  xlviii,  197. 
Sanders,   W.   E  :  Primary  Pulmonary  Arteriosclerosis  with  Hypertrophy  of  the  Right 

Ventricle,  Arch.  Int.  Med.,  Chicago,  1909,  iii,  257. 
Rogers,    L. :  Extensive   .\theroma  and   Dilatation   of  the   Pulmonary   Arteries,   without 

marked  Valvular  Lesions,  as  a  not  very  Rare  Cause  of  Cardiac  Disease  in  Bengal, 

Quart.  J.  Med.,  Oxford,  1908-9,  ii,  1. 
Brieger,  L.:  Clinical  Lectures  at  the  Hydrotherapeutische  Anstalt  der  Kgl.  Poliklinik, 

Beriin,  1906. 


ARTERIOSCLEROSIS.  269 

Riley:  Blatter  f.  klin.  Hydrotherap.,  1898;  cited  from  Buxbaum,  B.,  Lehrbuch  der  Hydro- 

therapie,  Leipz.,  1903. 
Senator,  H.:  Ueber  die  Arterioskelerose  und  ilire  Behandlung,  Therap.  d.  Begenw.,  Berl., 

1907,  xlviii,  97. 
Koranyi,  V.:  Ueber  die  Wirkung  des  lods  auf  die  durch  Adrenalin  erzeugte  Arterione- 

krose,  Deutsch.  med.  Wchnschr.,  Leipz.,  1908,  xxxii,  679. 
Boveri,   P.:  Contributo  alio  studio  degli  ateromi  aortici  sperimentali,  Clin.  med.  ital., 

Milano,  1906,  xlv,  41. 
Cummins,  W.  T.,  and  Stout,  P.  S.:  Experimental  Arteriosclerosis  by  Adrenalin  Inocula- 
tions and  the  Effect  of  Potassium  Iodide,  Univ.  Penn.  M.  Bull.,  Phila.,  1906-7,  xix,  101. 
Biland,  J.    Ueber  die  durch  Nebennierenpraparate  gesetzten  Gefass-  und  Organverander- 

ungen,  Deutsch.  x\rch.  f.  klin.  Med.,  Leipz.,  1906,  Ixxxvii,  413. 
Loeb,  L.,  and  Githens,  T.  C:  The  Effect  of  Experimental  Conditions  on  the  Vascular 

Lesions  produced  by  Adrenalin,  Am.  J.  M.  Sc,  Phila.  and  N.  York,  1905,  cxxx,  658. 
Loeb,  L.,  and  Fleisher,  M.  S.:  Influence  of  Iodine  Preparations  on  the  Vascular  Lesions 

Produced  by  Adrenalin,  ibid.,  1907,  cxxxiii,  903. 


XI. 

VASOMOTOR  CRISES  AND  THE  ANGIONEUROTIC  LESIONS. 

VASOMOTOR    CRISES. 
GENERAL    CONSIDERATIONS. 

The  general  clinical  manifestations  of  arteriosclerosis  bear  a  close 
relation  to  the  condition  described  by  Pal  as  "vasomotor  crises,"  under 
which  he  includes  all  conditions  which  are  associated  with  more  or  less 
sudden  constriction  or  dilatation  of  the  arteries,  and  whose  symptoms  and 
signs  disappear  or  markedly  diminish  as  soon  as  this  paroxysmal  change  in 
the  blood-vessels  passes  off.     There  are  accordingly 

(1)  Vasoconstrictor  crises,  usually  associated  with  hypertension, 

(2)  Vasodilator  (hypotension)  crises. 

The  vasoconstrictor  crises  Pal  divided  into 

(1)  Abdominal  type.  (2)  Pectoral  type.  (3)  Cerebral  type.  (4)  Crise.s  in  the  ex- 
tremities.   (5)  Crises  in  the  large  arteries. 

The  vasodilator  crises  according  to  Pal  include 

(1)  Ordinary  syncope.  (2)  Surgical  shock.  (3)  Collapse  after  infectious  disease 
or  most  poisonings.  (4)  Erythromelalgia  and  many  other  "trophic"  skin  disease.^  (5) 
Occasional  cases  of  tabes  with  lancinating  pains  and  low  blood-pressure.  (6)  Various 
attacks  of  weakness  in  Addison's  disease. 

Probably  no  unit  cause  exists  for  the  crises  themselves;  the  visceral 
crises  and  lancinating  pain  in  tabes,  the  painter's  colic,  the  uraemic  con- 
vulsion, the  delirium  of  the  cerebral  sclerotic,  the  pain  of  angina  pectoris, 
and  the  attack  of  cardiac  asthma  seem  to  have  little  etiology  in  common 
except  their  relation  to  the  sympathetic  nerves.  However,  all  manifest 
high  blood-pressure,  and,  according  to  Pal,  all  are  relieved  by  artificial 
depression  of  blood-pressure.  It  is,  therefore,  not  unlikely  that,  however 
diverse  the  ultimate  causes  of  the  condition,  the  cause  of  the  symptoms 
is  high  blood-pressure  with  localized  vasoconstriction.  The  variation  in 
the  areas  of  constriction  in  regions  whose  arteries  are  already  sclerotic 
accounts  for  the  occurrence  of  the  different  symptom  complexes. 

As  to  treatment,  the  statements  of  Pal  would  lead  one  to  believe  that 
they  are  all  relieved  by  vasodilators,  especially  nitro- 
glycerin and  the  nitrites,  occasionally  by  sodium  thiocyanate, 
and  that  marked  improvement  results  while  the  blood-pressure  is  lowered. 
The  symptoms  return  if  the  blood-pressure  again  rises.  (Pal,  also  Heitz, 
and  Norrero.)  However,  Prof.  Barker's  experience  at  the  Johns  Hopkins 
Hospital  does  not  warrant  such  sweeping  conclusions. 

'  Buerger's  studies  indicate  that  there  Are  organic  lesions  in  some  of  these  cases. 
270 


VASOMOTOR   CRISES. 


271 


Case  of  Abdominal  Vasomotor  Crises.     (Quoted  from  Pal.) 

P.  v.,  sausage  maker,  aged  57,  had  rheumatism  14  years  ago,  and  for  the  past  year 
pain  and  pressure  in  the  epigastrium,  especially  on  taking  a  deep  breath.  Has  occa- 
sional paroxysms  of  extreme  dyspnoea  and  palpitation  of  the  heart,  but 
always  has  some  shortness  of  breath.  He  was  formerly  a  heavy  drinker,  now  drinks  two 
or  three  litres  of  beer  a  day  as  well  as  a  half  litre  of  wine  and  some  whiskey!  He  also 
smokes  in  moderation. 

On  admission,  April  7, 1904,  he  was  found  to  be  a  well-nourished  man,  slightly  cyanotic. 
Lungs  clear,  respiration  34.  Heart.  Maximum  impulse  in  sixth  interspace  two  fingers' 
breadth  beyond  mammillary  line.  Dulness  extends  to  third  rib  above  and  two  fingers' 
breadth  beyond  the  right  margin  of  the  sternum.  Sounds  quite  clear  at  apex  and  base, 
second  aortic  sound  not  accentuated.  Pulse 
68;  radial  walls  stiff;  blood-pressure  225. 
Liver  enlarged;  spleen  not  palpable.  Slight 
oidema  of  feet  and  legs.  Urine  2600  c.c;  sp. 
gr.  1010;  albumin  1.5  Gm.  per  litre. 

Patient  was  given  0.5  Gm.  (gr.  viii)  so- 
dium thiocyanate  t.i.d.  to  diminish  his  blood- 
pressure. 

April  21.  Patient  delirious;  blood-pres- 
sure 110.  Thiocyanate  discontinued,  where- 
upon delirium  disappears.  The  chart  in  Fig. 
160  shows  the  course  of  the  blood-pressure, 
pulse-rate,  and  respiration.  The  patient  was 
free  from  other  exceptional  symptoms  from 
April  7  to  May  1.  May  1,  8.00-11.30  a.  m. 
Feels  hot  and  cold.  11.30.  Sudden  attack 
of  severe  pain  and  great  feeling  of  pressure 
in  epigastrium.  11.35.  Pains  in  back  and 
third  to  seventh  vertebrae.  Cries  out  with 
pain,  and  also  cries  "  I  am  choking."  Lungs 
clear.  Cardiac  dulness  only  to  right  sternal 
margin  and  to  two  fingers'  breadth  within 
left  mammillary  line.  11.40.  Symptoms 
diminish  but  pressure  in  epigastrium  still 
present.  11.41.  Symptoms  reappear.  11.42. 
Diminution  of  symptoms,  pains  less. 


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Fig.  160." 


-Blood-pressure  chart  of  P.  V. 
vasomotor  crisis. 


Typical 


A  second  severe  attack  as  before.  11.55. 
After  a  few  minutes  patient  has  a  third  momentary 
attack  with  blood-pressure  over  200  mm.  Hg,  which  then  subsides.  12.10. 
Feels  better.  12.55.  Still  better.  Free  from  attacks  until  May  3,  during  which  time  he 
receives  0.5  Gm.  (gr.  vii)  diuretin  t.i.d.  On  May  18,  sodium  thiocyanate  was 
again  given,  which  lowered  blood-pressure  but  caused  delirium. 
From  that  time  until  discharged  frequent  attacks  of  pain  and  hypertension. 

Pal  reports  similar  hypertensive  crises  in  association  with  the  colic  of 
lead  poisoning  and  also  with  the  visceral  crises  of  tabes, ^  the  pain  being 
always  relieved  when  the  blood-pressure  is  brought  down  by  amyl  nitrite 
or  nitroglycerin;  as,  for  example,  in  the  following  case. 

Case  of  Abdominal  Crisis  in  Lead  Poisoning. 

N.  J.,  painter,  aged  31,  has  had  lead  colic  twice  before.  Was  free  from  it 
on  change  of  occupation,  but  it  returned  when  he  again  worked  in  lead.  Drinks  little; 
denies  lues.     He  has   had  abdominal  pain  for  three  weeks.     During  past  few  days  has 


'  The  claim  of  Pal  that  a  similar  association  of  pain  with  high  blood-pressure  exists 
with  the  lancinating  pains  of  limbs  cannot  be  maintained,  since  the  pains  in  his  own  cases 
are  sometimes  associated  with  hypotension,  sometimes  with  hypertension. 


272 


DISEASES   OF   THE   HEART    AND    AORTA. 


had  continuous  cramps,  loss  of  appetite,  and  no  stool.  He  is  pale  and  has  a 
marked  lead  line.  Pupils  react  readily.  Lungs  clear.  Heart  normal;  pulse  rather  hard. 
Abdominal  walls  tense,  tender  on  both  sides.     Spleen  just  palpable. 


July  23.  8.30  p.m.    B.  P.  130.    Slight  pain. 

P.  68.     B.  P.  170.     Increased  pain. 

Amyl    nitrite    inhalation. 

No   pain. 

Pain  again,  lasting  then  over  one-half  hour  with  same  B.  P. 

After  amyl  nitrite,  which  again  gave  relief. 

Pains  return. 

Further  increase  of  pain. 

Pains   diminish   under   amyl    nitrite. 

They  return  again,  but 

Pains    disappear   under   amyl     nitrite. 

After  July  25,  blood-pressure  was  always  under  130  (during  last   four  days  under 
110),  the  patient  was  free  from  pain,  and  bowels  were  regular. 


8.30  P.M. 
9.10  P.M. 
9.13  P.M. 
9.1o  P.M. 
9.17  P.M. 
9.45  P.M. 
9.48  P.M. 

12  M. 
4.20  A.M. 


B.P 
B.  P 
B.P 
B.P 


B. 


105. 
165. 
95. 
140. 
160. 
P.  1.35. 


6..30  A.M.    B.  P.    8i 


Case  Illustrating  the  Cerebral  Crises. 

The  following  case,  illustrating  what  Pal  terms  the  cerebral  type  of  vascular  crisis, 
was  under  the  writer's  care  at  the  Johns  Hopkins  Hospital: 

J.  M.  C,  grocer,  aged  52,  who  had  suffered  repeatedly  with  myocarditis, 
hypertrophied  heart,    irregular   pulse,    and   general   anasarca,    entered   the   Johns 

Hopkins  Hospital  in  September,  1903. 

Oct.  24.  Restless  at  night.  Left  pupil 
larger  than  right:  both  react  normallj'. 
Nov.  2.  Very  weak.  Pulse  weak  and  irregu- 
lar.    Liver  enlarged. 

Nov.  5.  At  12.30  P.M.  began  to  complain 
of  general  discomfort  with  numbness  in  legs; 
complained  of  nervousness  and  restlessness. 
At  12.45  P.M.  the  restlessness  became 
very  marked;  he  began  to  strike  out  with 
his  hands  and  to  try  to  get  out  of  bed.  Was 
at  this  time  conscious  and  able  to  understand 
questions.  (Blood-pressure  curve  shown  in 
Fig.  161.)  No  aphasia.  Pupils  equal  and 
dilated.  Head  and  eyes  drawn  to  right  and 
rigid.  There  was  some  twitching  of  muscles 
of  both  arms  and  hands.  Reflexes  of  right 
arm  slightly  exaggerated.  Soon  became  cya- 
notic and  vessels  of  neck  stood  out.  Be- 
came unconscious.  Respiration  stertorous. 
Blood-pressure  270  mm.  Hg.  After 
600  c.c.  of  blood  had  been  withdrawn  from  left  arm,  cyanosis  slowly  subsided,  respira- 
tion becoming  less  stertorous  and  blood-pressure  falling  to  180  mm.  Hg. 

Becomes  conscious  after  catheterization  at  7.30  p.m.  Still  picking  at  bedclothes, 
which  continued  until  next  morning.  He  was  then  mentally  clear  by  11  a.m.  and  pupils 
reacted  to  light. 

Nov.  6.  9  P.M.  Remained  clear  and  recalled  hallucinations  of  previous  night, 
realizing  them  as  hallucinations.    Blood-pressure  160. 

Had  no  further  attacks  of  this  kind  and  blood-pressure  remained  below  190. 
Died  March  28,  1904.    Autopsy  showed  chronic  myocarditis  (heart  1000  Gm.),  chronic 
adhesive  pericarditis,  coronary  sclerosis,  hydronephrosis,  and  stone  in  right  kidney.' 

'  It  is  possible  that  this  attack  may  h^e  been  due  to  transitory'  cerebral  oedema 
like  that  described  by  H.  Gushing  and  James  Bordley  (Subtemporal  Decompression  in  a 
Case  of  Chronic  Nephritis  with  Uraemia;  with  Especial  Consideration  of  the  Neuroretinal 
Ivesion,  Am.  J.  M.  Sc,  1908,  cxxxvi,  484). 


150 


Fig.  161. — Blood -pressure  chart  showing  a  vascu- 
lar crisis  of  the  cerebral  type. 


VASOMOTOR   CRISES.  273 


INTERMITTENT    CLAUDICATION. 


This  condition  is  always  associated  with  sclerosis  of  the  femoral, 
popliteal,  or  one  of  the  other  arteries  of  the  leg  which  are  usually  pipe-stem 
in  character.  Often  the  atheromatous  changes  are  readily  demonstrable 
by  the  X-ray.  Owing  to  the  narrowed  lumen  of  the  artery,  the  amount 
of  blood  that  can  flow  through  it  is  limited, 
but  this  is  sufficient  to  supply  the  muscle  when 
at  rest.  During  slow  walking  the  COj  pro- 
duced by  the  muscle  and  the  oxygen  needed 
by  it  increase  greatly.  If  the  arterial  flow  is 
sufficient,  no  symptoms  appear;  but  when 
rapid  walking  or  running  is  begun,  there  is  a 
sudden  increase  in  the  oxidation  in  the  muscle, 
and,  since  the  blood  supply  cannot  keep  pace  fig.  i62.— Diagram  to  illustrate 
with  it,  asphyxia  of  both  the  muscle  and  its  l^' t^fZa'^TelotVt^rr^. 
nerve  endings  sets  in,  accompanied  by  paralysis     soUd  line  indicates  CO2  formation 

r  J.I.      ^•      V.  iPx         -J.  •  ••  r  during    halts    and    while    walking, 

of  the  hmb  and   often  intense  pam  arising  from        Broken  line  represents  the  rapidity 

stimulation  of  the  sensory  fibres  by  the  CO,.     °^  CO2  elimination.    *  indicates  the 

rrii  ,•       ,    •  11      1    ;       1      1,  TA       •  ,1  degree  of  CO2  accumulation  at  which 

Ihe  patient  is  compelled  to  halt.  During  the  pain  sensations  set  in. 
rest  the  CO2  production  falls,  and  the  slow  cir- 
culation is  able  to  carry  off  the  excess  and  to  supply  fresh  oxygen  to  the 
tissues.  With  the  renewed  aeration,  function  returns.  The  patient  is  able 
to  walk  again  until  local  asphyxia  sets  in;  and,  since  this  will  be  brought 
about  by  the  same  amount  of  COj  as  before,  his  walking  will  be  limited  to 
the  same  distance.    He  must  travel  in  stages.    (Fig.  162.) 

Case  of  Intermittent  Claudication. 

H.  E.,  carpenter,  aged  74,  complains  of  pain  in  right  foot,  drinks  beer  and  whiskey 
in  moderation,  smokes  very  little,  and  has  always  been  healthy.  In  October  toe  was  red 
and  ached.  For  the  past  ten  or  fifteen  years  patient  has  been  at- 
tacked by  severe  pains  in  both  feet,  causing  him  to  stop  in  his 
walks.  Knees  never  gave  way.  The  attacks  came  on  oftenest  during  exercise.  On 
examination,  thorax  is  emphysematous;  heart  slightly  enlarged  to  left.  Blowing  systolic 
murmur  heard  over  the  tricuspid  area,  becoming  musical  over  the  apex,  well  heard  in  the 
axilla,  but  faint  and  blowing  in  the  pulmonary  area,  where  the  second  sound  is  accentuated. 
Pulse  slightly  irregular.  Right  radial  more  sclerotic  than  left.  Blood-pressure  165  mm. 
General  reddening  from  tarsometatarsal  joints  to  the  toes  of  right  foot,  where  pulsa- 
tion of  dorsalis  pedis  is  not  felt.  Both  tibials  are  palpable,  but  pulsation 
is  well  felt.     Left  foot  normal,  artery  pulsating  well.     Both  popliteals  are  very  sclerotic. 

Given  nitroglycerin  mg.  1  (gr.  ^\)  t.i.d.,  alternating  with  sodium  nitrite  0.2  Gm. 
(gr.  iii)  t.i.d.  He  was  somewhat  improved  by  treatment,  but  left  the  hospital  a  few 
days  later. 

Prognosis. — Since  the  claudication  is  simply  part  of  the  general  arterio- 
sclerosis, the  prognosis  is  bad,  for  the  coronary  arteries,  aorta,  and  cerebral 
arteries  may  be  involved.  Sometimes,  however,  the  arterial  change  is 
confined  to  the  limbs,  occurring  simply  as  degeneration  of  the  media  with 
atheroma,  exactly  as  is  found  in  experimental  adrenalin  arteriosclerosis. 
In  that  case  the  prognosis  as  to  life  is,  of  course,  better. 


18 


274  DISEASES    OF   THE    HEART    AND    AORTA. 


HYPOTENSIVE    VASOMOTOR    CRISES. 

The  so-called  "  hypotensive  "  crises  seem  to  bear  no  relation  to  arterio- 
sclerosis, but  rather  to  trauma,  action  of  toxic  substances,  and  perhaps 
to  cutaneous  diseases.  They  are  in  the  main  associated  with  depression 
of  the  vasomotor  system  and  have  been  discussed  elsewhere.  The  one 
condition  with  paroxysmal  depression  of  the  blood-pressure  which  may 
owe  its  origin  to  arteriosclerosis  is  paroxysmal  tachycardia  (see  page 
560). 

ANGEIONEUROSES. 

Maurice  Raynaud  in  1862  described  many  cases  of  this  group,  espe- 
cially of  the  condition  which  bears  his  name.  He  showed  that  the  three 
phenomena  manifested  in  these  conditions  are: 

1.  Local  syncope,  i.e.,  blanching  from  absence  or  diminution 
of  blood  in  the  arteries  of  the  part  affected; — Raynaud's  disease  a  spas- 
modic vasoconstriction.  This  is  usually  symmetrical  in  its  distribution, 
affecting  the  ends  of  the  extremities,  i.e.,  toes,  hands  or  feet,  arms  or  legs. 
The  trouble  in  one  extremity  is  frequently  more  intense  than  in  the  other. 
Often  it  leads  to  formation  of  bullae,  ulceration,  and  to  symmetrical  gangrene 
(Raynaud's  disease). 

2.  Local  asphyxia,  i.e.,  presence  of  a  venous  blood,  that  is  to 
say  of  a  blood  insufficiently  oxygenated,  causing  blueness  of  the  part  (now 
designated  as  acrocyanosis)  with  a  distribution  corresponding  to  that  of 
Raynaud's  disease. 

3.  Local  hyperaemia,  giving  rise  to  redness  (as  in  the  condi- 
tion termed  erythromelalgia  by  Weir  Mitchell). 

Later  investigations  have  enabled  Cassirer  as  well  as  Barker  and 
Sladen  to  epitomize  the  symptoms  of  vasomotor  disease  as  follows: 

The  vasomotor  symptoms  include  (1)  hyperemia,  (2)  syncope,  and  (3) 
asphyxia;  the  sensory,  (1)  pain,  (2)  hyperaesthesia,  (3)  ansesthesia,  (4) 
paraesthesia ;  the  trophic,  (1)  ulceration,  (2)  gangrene,  (3)  dystrophies 
of  the  skin  (Barker  and  Sladen).  They  affect  the  fingers  and  particularly 
the  toes.  The  chief  types  of  disease  are  acrocj^anosis  (Cassirer),  erythro- 
melalgia (Weir  Mitchell),  and  Raynaud's  disease. 

The  symptoms  may  be  arranged  as  follows  in  ascending  scale  (Barker 
and  Sladen) : 

1.  Acrocyanosis. 

Vasomotor  symptoms — venous   stagnation   and    hyperaemia  in   fingers  and 
toes  with  cyanosis;    sensory  and  trophic  disturbances  absent. 

2.  Acroparaesthesia. 

Acrocyanosis — sensory  symptoms  (paraesthesia),  numbness,  pain,  and  tingUng. 

3.  Erythromelalgia. 

Vasomotor — hyperaemia  (arterial).     Sensory — pain. 

4.  Raynaud's  disease  (all  the  symptoms). 

Vasomotor — hyperaemia,  syncope,  and  asphyxia.     Sensory — pain,  anaesthesia, 
paraesthesia.     Trophic — gangrene  and  scleroderma. 

As  might  be  expected,  there  are  many  cases  with  symptoms  inter- 
mediate between  these  groups  and  many  transitions  from  one  to  the  other 
(Sachs). 


ANGEIONEUROSES.  275 

Pathology. — Raynaud  realized  that  the  gangrene  in  the  disease  which 
bears  his  name  differed  from  ordinary  gangrene  and  directed  his  first  inves- 
tigations to  the  state  of  the  arteries.  He  found  that,  though  the 
pulse  became  very  small  or  impalpable  during  the 
attacks  of  blanching,  it  returned  to  normal  volume 
between  attacks.  He  made  very  careful  pathological  studies  of 
the  extremities  in  a  number  of  cases,  and  finding  the  arteries  clear  con- 
cluded that  the  trouble  was  of  vasomotor  origin,  a  view  which  he  supported 
by  demonstrating  transitory  changes  of  caliber  in  the  radial,  popliteal, 
and  retinal  arteries,  associated  with  the  attacks.  In  accordance  with  these 
studies  of  Raynaud  the  vasodilation  of  erythromelalgia  corresponds  to  a 
period  of  paralysis  of  the  vasoconstrictor  nerves  (sympathetic  paralysis) 
quite  similar  to  the  active  hyperaemia  which  Claude  Bernard  produced  in 
the  rabbit's  ear  by  cutting  the  cervical  sympathetic.  Just  such  a  local 
paralysis  x)f  the  vasomotors  produced  by  the  overheating  of  a  hand  or  foot 
benumbed  by  cold  gives  rise  to  the  condition  of  ''chilblains."  The  latter 
condition  is  always  associated  with  overheating  after  exposure  to  cold 
and  often  with  formation  of  blebs,  w'hile  attacks  of  erythromelalgia  may 
occur  spontaneously  from  slight  emotional  or  nervous  disturbances  or  from 
slight  exposure  to  cold  without  overheating.  There  is  rarely  bleb  forma- 
tion. An  attack  of  chilblains  induced  by  overheating  may  thus  be  con- 
tinued in  spontaneous  attacks  of  erythromelalgia. 

Raynaud's  disease.'on  the  other  hand,  corresponds 
to  an  extreme  vasoconstriction,  like  that  produced 
in  ergotism.  Raynaud  himself  was  so  much  impressed  with  this 
similarity  that  he  made  searching  inquiries  in  all  his  cases  regarding  the 
character  of  rye  bread  taken,  and  conducted  an  extensive  series  of  experi- 
ments upon  ergotism  in  various  animals.  He  was  forced  to  discard  the  ergot 
hypothesis  by  the  absence  of  any  obtainable  evidence  of  ergot  ingestion, 
but  the  parallelism  between  the  two  conditions  remains. 

Case  of  Mild  Raynaud's  Disease. 

A.  S.,  a  trained  nurse,  aged  30,  was  always  healthy  until  the  age  of  nineteen,  when 
during  her  period  of  training  she  was  compelled  to  have  a  small  ovarian  cyst  and  one 
ovary  removed.  For  some  years  she  suffered  considerable  pain  from  adhesions,  so  that 
three  years  ago  these  were  broken  up  by  a  second  operation.  She  bore  the  operation 
well,  but  during  convalescence  three  weeks  later  had  a  fainting  spell,  since  when  she 
suffers  from  severe  palpitation.  For  the  past  two  years  she  has  found  that  in  cold  weather 
both  her  hands  and  forearms  become  absolutely  white,  cold,  and  numb.  This  condition  is 
soon  relieved  by  rubbing  or  by  laying  them  in  a  basin  of  warm  water,  but  is  sufficiently 
severe  to  prevent  her  from  accepting  a  very  desirable  appointment  in  a  colder  climate. 

Between  attacks  the  patient  seems  perfectly  healthy,  has  a  good  color.  All  the  arteries 
are  soft.  They  appear  to  be  of  normal  caliber  and  pulsate  normally.  The  heart  is  normal 
in  size  but  moves  7  cm.  from  left  to  right  as  the  patient  turns  from  one  side  to  the  other. 
The  right  kidney  is  also  palpable  and  very  movable.  The  rest  of  the  abdomen  and  the 
lungs  are  clear.  The  blanching  of  the  hands  occurs  less  frequently  and  less  intensely  when 
the  patient's  health  is  good,  but  it  occurs  much  more  frequently  when  the  patient  is  excited. 

Nitrites,  belladonna,  digitalis,  bromides,  and  a  large  number  of  cardiac  stimulants 
have  been  tried  by  the  patient  without  marked  effect. 


276 


DISEASES   OF   THE   HEART    AND    AORTA. 


THROMBOANGITIS     OBLITERANS. 

In  recent  years  Weiss  and  v.  Winiwarter,  and  especially  L.  Buerger, 
have  discovered  a  group  of  cases  in  which  symptoms  at  times  simulating 
those  of  the  vasomotor  trophoneuroses  are  produced  by  complete  occlu- 
sion of  the  arteries  or  veins  with  spontaneous  thrombosis  (thromboangitis 
or  thrombophlebitis  obUterans).  In  such  cases  the  largest  artery  and 
sometimes  both  artery  and  vein  become  occluded  by  a  thrombotic  process 
of  considerable  extent.  After  a  short  time  the  fresh  red  thrombi  within 
the  vessels  undergo  organization,  usually  with  permanent  obliteration  of 
the  lumen  by  white  fibrous  tissue.  There  is  no  proliferation  of  new  elastic 
fibres  encroaching  on  the  lumen  as  is  the  case  in  arteriosclerosis 
(Fig.  163),  though  a  few  elastic  fibres  are  found  in  the  newly  formed  blood- 
vessels. 


-t'>'«B^5^-^- 


Fig.  163. —  i  in.juiu.jaugiu.-  obliterans  (A)  and  endarteritis  obliterans  vB;.  (After  Buerger.)  The 
elastic  fibres  (stained  black)  are  absent  from  the  organized  thrombus  in  A  but  present  in  large  numbers  in 
the  arterioscleriotic  lesion  B. 


This  was  the  condition  first  sought  for  by  Raynaud  to  explain  the 
origin  of  symmetrical  gangrene,  and  described  by  him  under  the  head  of 
senile  gangrene.  In  Buerger's  experience  of  over  70  cases,  however,  it  is 
most  frequent  in  Russian  and  Polish  male  Hebrews  between  twenty  and 
thirty-five  or  forty,  and  hence  is  usually  a  ''presenile"  gangrene.  In 
such  cases  the  local  syncope  and  ulceration  are  due  to  arterial  occlusion. 
The  red  blush  is  due  to  compensatory  capillary  dilatation  (termed  eryth- 
romelia  by  Buerger,  in  contrast  to  erythro melalgia) .  Cyanosis  of  the  limb 
occurs  when  the  venous  circulation  is  slowed  from  any  cause. 

The  sensory  disturbances  found  in  the  trophoneuroses  are  also  found 
in  thromboangitis  obliterans. 

The  clinical  picture  produced  by  thromboangitis  obliterans  is  some- 
times so  similar  to  that  of  Raynaud's  disease  (spasmodic  vasoconstriction) 
that  Buerger  has  found  some  undoubted  cases  of  the  former  condition 
reported  in  the  Uterature  as  cases  of  the  latter. 

Differentiation  between  Thromboangitis  Obliterans  and  Angeioneuroses. — ^Dr.  Buerger 

has  informed  the  writer  that  he  finds  the  following  points  useful  for  clinical  differentiation: 
1.  There  is  always  at  least  one   vessel    which    remains    permanently 
pulseless,    while  in  Raynaud's  disease  the  pulse  soon  returns  to  normal. 


THROMBOANGITIS  OBLITERANS. 


277 


2.  Intermittent   claudication   is  present  in  most  of  the  cases. 

3.  Usually  one  limb  is  affected  a  considerable  time  before  the  other,  and 
the  disease  usually  attacks  the  lower  extremities. 

4.  There  are  exacerbations,  but  they  come  on  and  subside  rather 
gradually  and  are  not  paroxysmal  like  Raynaud's  disease. 

5.  Limbs  which  are  red  (erythromelia)  or  blue  in  the  dependent  position  become 
blanched    and    ischaemic    when   elevated. 

6.  Migrating  phlebitis  is  not  infrequently  associated  with  thromboangitis  obliterans. 

7.  He  has  seen  over  70  cases  in  Russian  and  Polish  male  Hebrews,  but  never  in  a 
female.    Raynaud's  disease  occurs  more  often  in  females. 

8.  Onset   is   usually  gradual,  while  it  is  sudden  in  Raynaud's  disease. 

9.  The  circulatory  phenomena  are  for  the  most  part  not  of  "vasomotor"  origin, 
but  are  due  to  occlusion  of  vessels.    They  therefore  bear  the  stamp  of  permanency. 

Nevertheless,  Dr.  Buerger  has  found  a  number  of  cases  in  which  the 
cUnical  differentiation  from  Raynaud's  disease  was  very  difficult.  Dr. 
Bernard  Sachs,  on  the  other  hand,  believes  that  the  vasomotor  neuroses 
manifest  themselves  in  diseased  blood-vessels  as  well  as  in  healthy  ones, 
and  that  the  pathological  diagnosis  of  endarteritis  or  thromboangitis  does 
not  exclude  the  clinical  diag- 
nosis of  erythromelalgia  or 
Raynaud's  disease.  Indeed  it 
is  readily  conceivable  that 
thrombosis  should  occur  more 
readily  in  somewhat  diseased 
arteries  than  in  normal  ones. 
Even  Dr.  Buerger  has  found 
some  intimal  changes  in  his 
cases.  Vasoconstriction  may 
also  favor  thrombosis.  More- 
over vasoconstriction,  arterial 
disease,  and  the  formation  of 
agglutinative  thrombi  may,  as 
is  seen  in  ergot  poisoning,  all 
be  produced  by  the  action  of  a 
single  toxic  agent. 

Case  of  Thromboangitis 
Obliterans. 

The  following  is  the  history  of 
a  case  which,  though  at  the  time 
diagnosed  as  Raynaud's  disease  and 
manifesting  many  symptoms  of  the 
latter,  in  the  light  of  Buerger's  in- 
vestigations appears  to  be  one  of 
thromboangitis  obliterans. 

H.  F.,  tailor,  aged  32,  admitted  April  14,  1903,  complaining  of  sore  toes  and 
sore  fingers.  Had  rheumatism  at  12  years;  otherwise  well.  Smokes  ten  cigarettes 
daily.  In  December,  1899,  cold  began  to  cause  a  burning  sensation  in  big  toe  of 
right  foot.  In  March,  1900,  pus  collected  under  the  base  of  nail.  The  nail  was 
removed,  and  four  months  later  the  entire  toe.  Wound  did  not  heal  well.  After  this, 
tingling  in  other  toes  when  out  of  doors,  never  when  indoors.  In  April, 
1902,  the  fingers  and  thumb  of  the  right  hand  began  to  tingle  and  become  painful,  and  a 
little  later  on  those  of  the  left  hand.  In  January,  1903,  the  left  big  toe  began  to  become 
gangrenous. 


Fig.  1G4. — Hauds  and  feet  of  a  patient  with  thrombo- 
angitis obliterans,  showing  gangrenous  ulcers  and  the 
stumps  of  amputated  toes.  The  arrows  point  to  the  gan- 
grenous ulcers. 


278  DISEASES   OF   THE    HEART    AND    AORTA. 

Physicial  examination  on  entrance,  negative  except  for  the  extremities.  Both 
hands  are  flushed,  not  blue,  not  tender,  but  there  is  some  deformation  of  the 
second  phalanx  of  the  middle  fingers.  Right  big  toe  missing;  sloughs  between  third  and 
fourth  digits.     Left  great  toe  necrotic;    tenderness  and  pain  over    both  first  metatarsals. 

Patient  complains  of  paroxysms  of  intense  pain  during  the  night,  lasting 
five  to  ten  minutes.  Elevation  of  the  limb,  warm  dressings,  massage,  were  a.l  without 
effect.  Condition  became  worse  in  spite  of  hot  HgCl^  compresses,  etc.,  and  the  left  great 
toe  had  to  be  removed.  The  stump  did  not  heal  for  several  months.  There 
was  never  pulsation  in  either  popliteal;  very  little  in  either 
femoral.     Patient  discharged  in  February,  1904,  unimproved. 

During  this  time  blood  count:  red  blood-corpuscles  5,000,000-5,500,000.  Haemo- 
globin 100  per  cent.    Urine  normal.    Blood-pressure  100  to  130  mm.  Hg.    Pulse  80. 

The  following  history  represents  a  more  typical  case  of  thromboan- 
gitis  obliterans  (quoted  from  Buerger). 

M.  K.,  44  years,  Russian  Hebrew,  father  of  three  healthy  children,  was  admitted  to 
Mt.  Sinai  Hospital  on  December  8,  1908.  His  limbs  never  troubled  him  until  about  a  year 
ago,  when  he  felt  the  presence  of  tender  spots  on  the  inner  side  of  the  right  foot.  Soon  other 
hard  "lumps"  and  "cords"  appeared;  some  of  these  in  the  neighborhood  of  the  ankle, 
others  higher  up  on  the  leg.  After  two  months  these  disappeared,  only  to  recur  after  a  very 
short  interval.  Since  then  he  has  never  been  absolutely  free  from  peculiar  "painful  spots," 
and  now,  on  admission,  he  still  has  signs  of  some  of  them.  About  three  months  after  the 
onset  of  these  symptoms  he  experienced  pain  in  the  big  toe,  especially  on  walking.  This 
has  become  gradually  worse,  so  that  he  has  been  unable  to  get  about  properly  for  almost 
two  months.  Of  late  he  has  often  had  cramps  in  the  calf  and  instep  of  the  right  leg  after 
walking  for  a  short  distance.  His  chief  complaint,  however,  is  the  painful  condition  of  the 
inner  side  of  his  right  leg. 

Physical  examination  showed  evidences  of  circulatory  disturbance  in  the  right  lower 
extremity.  Both  the  dorsalis  pedis  artery  and  the  posterior  tibial  were  pulseless,  although 
pulsation  of  both  the  femoral  and  posterior  tibial  artery  could  be  easily  detected. 

Over  the  inner  border  of  the  right  foot  there  is  a  red  streak  about  one-half  inch  in 
length.  This  corresponds  to  a  tender  indurated  mass  which  thins  out  and  is  lost  as  it  is 
traced  upward.  A  short  distance  below  the  middle  of  the  leg  the  upper  end  of  a  hard  cord 
can  be  palpated.  This  extends  down  behind  the  border  of  the  tibia  for  more  than  two 
inches,  is  adherent  to  the  skin,  somewhat  nodulated,  and  marks  the  centre  of  an  area  of 
hypersensitive,  swollen,  turgid  skin.  There  are  no  trophic  disturbances.  Diagnosis  : 
Ihromboangitis  and  thrombophlebitis  of  the  internal  saphenous  and  some  of  its  tributaries. 

On  December  15,  1908,  a  portion  of  the  thrombosed  saphenous  was  removed  for 
pathological  examination. 

On  December  26,  1908,  the  physical  examination  was  recorded  as  follows:  In  the 
horizontal  position,  the  right  foot  has  a  light  shade  of  red;  this  is  most  marked  over  the 
big  toe  and  fades  off  towards  the  ankle.  In  the  web  between  the  third  and  fourth  toes 
there  is  a  superficial  ulcer.  On  the  inner  side  of  the  foot  almost  two  inches  from  the  internal 
malleolus  there  is  a  hard,  cord-like  nodule  which  is  adherent  to  the  skin.  Behind  the  tibia 
there  is  the  scar  left  after  removal  of  a  portion  of  the  saphenous  vein.  The  saphenous  can 
no  longer  be  felt. 

On  elevation  of  the  foot  blanching  sets  in  rapidly  and  pain  becomes  intense.  The 
pendent  foot  turns  very  red  (marked  erythromelia) . 

Further  Course. — February  15,  1909,  the  pain  in  the  foot  has  been  getting  steadily 
worse,  and  the  fourth  toe  is  beginning  to  turn  black.  On  the  2.3d  of  February  amputation 
at  the  knee  was  done,  at  the  request  of  the  patient,  for  early  gangrene  of  the  fourth  toe. 

TREATMENT. 

In  the  light  of  Buerger's  pathological  studies,  treatment  should  be 
directed  toward  keeping  up  a  rapid  circulation  through  the  part  and  dimin- 
ishing the  tendency  to  coagulate.  To  bring  about  the  former  the  vasodilator 
drugs,  especially  the  nitrites,  should  be  freely  used,  but  most  of  all  the 


THROMBOANGITIS   OBLITERANS.  279 

mechanical  methods  of  inducing  arterial  hypersemia, — hot  poultices, 
mustard  foot  or  hand  baths,  or  the  Bier's  hypersemia  by  suction  in  vacuo 
(not  Bier's  stagnation  hypersemia).  Exsanguination  of  the  arm  or  leg 
with  the  Esmarch  bandage,  which  has  been  advocated  by  some  writers, 
has  given  but  little  clinical  encouragement;  and  in  the  light  of  the  recent 
pathological  studies  seems  to  be  the  worst  possible  procedure,  since  it 
provokes  the  stagnation  it  intends  to  cure,  at  least  long  enough  to  induce 
further  thrombosis. 

It  is  possible  that  the  administration  of  sodium  citrate  by  mouth,  in 
doses  sufficient  to  slow  the  coagulation  time  of  the  blood,  might  aid  in 
diminishing  the  tendency  to  intravascular  coagulation,  but,  since  the  fibrin- 
ferment  is  supplied  on  the  spot  from  the  cells  of  the  intima,  it  is  probable 
that  this  would  not  be  of  much  avail. 

To  keep  up  arterial  hypersemia  until  the  thromboangitis  has  been 
repaired  is  the  only  hope  in  therapy. 

From  the  time  of  Raynaud  to  the  present  excellent  results  have  been 
reported  from  the  use  of  warm  (but  not  too  hot)  poultices. 

BIBLIOGRAPHY. 

Vasomotor  Crises  and  Angioneuroses. 

Pal,  J.:  Die  Gefa.sskrisen,  Leipz.,  1905. 

Charcot,  J.  M.:  Sur  la  claudication  intermittente  observee  dans  un  cas  d'obliteration  com- 
plete de  lime  des  arteres  iliaques  primitives,  Compt.  rend.  Soc.  de  Biol.,  Paris,  1857, 
2  serie,  xii,  225.  Sur  la  claudication  intermittente  par  obliteration  arterielle,  Progr^s 
Med.,  Paris,  1887. 

Erb,  W.:  Ueber  das  "  intermittirende  Hinken"  und  andere  nervosa  Storungen  infolge  von 
Gefiiss  erkrankungen,  Deutsch.  Ztschr.  f.  Nervenheilk.,  xiii,  1.  Ueber  Dysbasia  angio- 
sclerotica,  Muenchen.  med.  Wchnschr.,  1904,  li,  905. 

Barker,  L.  F.,  and  Sladen,  F.  J.:  On  Acrocyanosis  Chronica  Anaesthetica  with  Gangrene, 
etc.,  J.  Nerv.  and  Ment.  Dis.,  N.  York,  1907,  xxxiv,  745. 

Cassirer,  R.:  Die  Vasomotorische  Trophoneurosen,  Berl.,  1901. 

Mitchell,  S.  Weir:  Phila.  M.  Times,  1872;  quoted  from  Sachs.  Mitchell,  S.  W.,  and  Spiller, 
W.  G.:  A  Case  of  Erythromelalgia  with  Microscopical  Examination  of  the  Tissue 
from  an  Amputated  Toe,  Am.  J.  M.  Sc,  Phila.,  1899,  N.  S.  cxvii,  1. 

Raynaud,  A.  G.  M.:  De  I'asphyxie  locale  et  de  la  gangrene  symetrique  des  extremites. 
Par.,  1862;  also,  On  Local  Asphyxia  and  Symmetrical  Gangrene  of  the  Extremities, 
Transl.  by  T.  Barlow,  Lond.,  1888. 

Buerger,  L.:  Thromboangiitis  ObHterans;  a  Study  of  the  Vascular  Lesions  leading  to 
Presenile  Gangrene,  Am.  J.  M.  Sc,  Phila.  and  N.  York,  1908,  cxxxvi,  567.  The  Veins 
in  Thromboangiitis  Obliterans,  with  Particular  Reference  to  Arteriovenous  Anas- 
tomosis as  a  Cure  for  the  Condition,  J.  Am.  M.  Asso.,  Chicago,  1909,  Hi,  1319. 

Sachs,  B.:  Raynaud's  Disease,  Erythromelalgia,  and  the  Allied  Conditions,  in  their 
Relation  to  Vascular  Disease  of  the  Extremities,  Am.  J.  M.  Sc,  Phila.  and  N.  York, 
1908,  cxxxvi,  560. 

Also,  Strauss,  H.:  Ueber  angiospastische  Gangran  (Raynaud'sche  Krankheit),  Arch.  f. 
Psychiat.,  Berl.,  1905,  xxxix,  109. 


XII. 

SCLEROSIS  OF  THE  CORONARY  ARTERIES,   AND   ANGINA 

PECTORIS. 

PHYSIOLOGY   OF   THE   CORONARY  CIRCULATION. 

The  coronary  arteries  have  usually  been  considered  to  be  terminal  arteries  in  the 
sense  of  Cohnheim;  that  is,  that  their  branches  did  not  anastomose  with  one  another  suffi- 
ciently to  maintain  an  adequate  circulation,  and  infarction  follows  their  occlusion.  This 
is  correct  under  most  clinical  conditions;  and  Porter  has  found  experimentally  that  the 
infarction  is  proportional  to  the  size  of  the  ligated  branch.  In  many  cases  ligation  of  a  coro- 
nary gives  rise  to  fibrillary  contractions  and  sudden  death  (Porter,  Magrath  and  Kennedy, 
Kronecker) ;  in  others  death  may  follow  within  a  few  minutes  (Cohnheim  and  v.  Schulthess- 
Rechbei^),  within  an  hour  (Panum),  or  the  animal  may  Uve  several  weeks  or  more 
(Baumgarten)  if  the  operation  is  done  aseptically.    Death  even  then  often  occurs  suddenly. 


'''''^''Ifr'^^ 


Fio.  165. — ^Efifect  of  ligation  of  a  large  coronary  artery  upon  the  blood-pressure.    (After  Cohnheim  and  v. 
Schulthess-Rechberg.)     Ck>ronary  artery  ligated  at  a. 

Distribution  of  the  Coronary  Arteries. —  Walter  Baumgarten  in  Porter's  laboratory 
was  able  to  ligate  the  various  coronary  branches  of  cats  and  dogs  under  aseptic  precau- 
tions and  produced  infarcts  in  the  corresponding  areas  of  the  myocardium.  He  found 
the  following  efifects  by  Ugating  the  various  branches: 

Ramus  descendens:  Anterior  wall  of  left  ventricle,  anterior  papillary  mus- 
cle, left  half  of  the  thickness  of  the  inter\'entricular  septum. 

Ramus  circumflex  us:  Posterior  wall  of  left  ventricle,  apex,  ix)sterior  papil- 
lary muscle,  a  certain  extent  of  the  right  ventricle,  posterior  wall  of  left  atrium,  posterior 
third  of  the  septum. 

Ramus  septi:  This  is  given  off  in  the  dog  near  the  origin  of  the  ramus  descen- 
dens or  independently  of  it.  Ligature  produces  a  triangular  infarction  with  the  apex  of  the 
triangle  towards  the  ligature. 

Right  coronary:  Greater  part  of  right  ventricle,  posterior  portion  of  the 
appendix  atrii.     (The  smaller  branches  of  the  atria  are  not  caught  in  the  ligature.) 

Baumgarten  also  excised  the  anaemic  area  and  perfused  it  with  defibrinated  blood, 
and  found  this  region  was  able  to  resume  contractions  when  the  cir- 
culation was  renewed  within. six  to  eleven  hours  after  the  artery  had  been  ligated.  The 
region  of  the  centre  of  the  infarct  lost  its  contractility  before  that  near  the  periphery, 
indicating  that  a  certain  degree  of  collateral  circulation,  perhaps  through  the  vessels  of 
Thebesius,  had  taken  place.  This  work  explains  why  it  is  that  a  certain  time  elapsed 
between  the  obstruction  of  the  artery  and  the  sudden  cessation  of  beat  in  the  experi- 
280 


SCLEROSIS   OF   THE   CORONARY   ARTERIES.  281 

ments  of  Panum  and  of  Cohnheim  and  v.  Schulthess-Rechberg.  The  greater  number  of 
Baumgarten's  dogs  and  cats  survived  the  operation  well  and  showed  no  change  in  heart 
action  beyond  a  transitory  arrhythmia  lasting  twenty-four  to  thirty-six  hours.  The 
sounds  were  normal  in  every  respect  and  possessed  no  undue  valvular  quality. 
Only  two  animals  showed  signs  of  sudden  cardiac  failure,  one  dying  in  the  midst 
of  violent  exertion  and  the  other  soon  after  it,  exactly  as  occurs  in  man  (see 
page  284). 

Hirsch  and  Spalteholz  found  that,  though  infarcts  were  produced  by  ligation  of  the 
coronary  artery,  the  infarcts  were  smaller  than  the  area  supplied  anatomically  by  the 
artery,  and  there  was  a  not  inconsiderable  amount  of  anastomosis,  especially  between  the 
branches  near  the  surface  of  the  heart.  In  man  Chiari  has  found  complete  occlusion  of 
the  right  coronary  artery  without  infarction,  and  Pagenstecher  has  ligated  that  artery 
in  an  operation  without  evil  result.  These  are  the  main  facts  regarding  the  coronary  circu- 
lation which  throw  light  upon  the  clinical  conditions  observed. 

Pratt  has  shown  that  the  excised  mammahan  heart  can  be  nourished 
through  the  veins  of  Thebesius  sufficiently  to  carry  out  forcible  contrac- 
tions for  a  considerable  time,  though  this  probably  is  not  the  case  in  the 
living  animal. 

It  has  long  been  a  matter  of  debate  whether  the  heart  muscle  was 
nourished  with  blood  during  the  systolic  or  during  the  dias- 
tolic period;  the  earliest  contention  being  that  of  Scaramucci  (1689)  that  the  coro- 
nary vessels  are  squeezed  empty  by  the  contraction  of  the  heart  muscle-fibres  during  systole 
and  fill  from  the  larger  and  more  superficial  coronary  vessels  during  diastole.  After  a  long 
controversy,  during  which  Rabatel  showed  that  the  curve  of  coronary  blood-pressure  and 
apparently  also  the  curve  of  blood  velocity  were  exactly  similar  to  the  curve  in  the  aorta, 
the  question  was  definitely  settled  upon  the  excised  heart  by  Porter  and  his  pupils 
in  favor  of  the  old  view  of  Scaramucci.  They  also  found  that  the  blood  in  the  coronary 
veins  is  squeezed  out  in  diastole. 

The  existence  of  vasomotor  nerves  for  the  coronaries  has  been  proved 
by  Maass,  who  found  that  the  vagus  exerted  a  vasoconstrictor,  the  accel- 
erator a  vasodilator  action  upon  these  vessels. 

This  was  confirmed  by  O.  Langendorff  and  Wiggers,  who  found  also  that  adrenalin 
exerted  a  vasodilator  action  upon  the  coronary  arteries  of  the  excised  heart  instead  of  its 
usual  vasoconstrictor  action.  Both  Wiggers  and  G.  S.  Bond  have  found  that  the  outflow 
through  the  coronary  veins  of  the  dog's  heart  in  situ  is  increased  by  the  administration 
of  adrenalin.  Bond  investigated  the  effects  of  a  large  number  of  other  drugs  as  well,  and 
found  that  the  coronary  outflow  always  followed  the  curve  of  general  blood-pressure;  so 
that,  under  the  experimental  conditions,  he  was  unable  to  demonstrate  any  specific  action 
upon  the  coronary  vessels,  even  from  doses  far  larger  than  would  be  administered  in  thera- 
peutics. However,  the  operation  is  so  severe  that  the  animals  are  always  in  profound 
shock. 

Ida  Hyde  in  Porter's  laboratory  found  that  the  coronary  blood  flow  was  diminished 
by  distention  of  the  heart,  a  fact  which  may  account  for  the  weaker  contraction  of  over- 
dilated  hearts. 

SCLEROSIS    OF   THE    CORONARY    ARTERIES. 

PATHOLOGICAL    ANATOMY. 

While  the  sclerosis  of  the  coronary  arteries  does  not  differ  in  its  pathol- 
ogy from  the  sclerosis  of  arteries  elsewhere,  nevertheless  the  action  upon 
the  heart  gives  rise  to  clinical  and  to  secondary  pathological  conditions 
which  are  quite  different  from  those  of  general  arteriosclerosis,  and  which 
therefore  deserve  special  consideration. 


282 


DISEASES   OF   THE   HEART   AND   AORTA. 


Another  important  condition  which  is  very  common  is  arterioscle- 
rotic or  atheromatous  change  arising  in  the  aorta  with  or  without  associated 
involvement  of  the  coronaries  themselves,  but  spreading  so  as  to  involve 
the  mouths  of  the  coronaries  as  they  arise  from  the  aorta,  and  strangu- 
lating these  vessels  as  they  pass  through  the  aortic  wall  (see  Fig.  166). 
This  has  the  same  effect  as  a  metal  band  constricting  an  artery  would  have; 
namely,  of  diminishing  the  blood-pressure  and  the  velocity  of  flow  in  the 
artery  beyond  it,  of  allowing  the  walls  of  the  artery  to  contract  down  and 
hence  of  producing  a  further  permanent  secondary  narrowing  of  the  lumen, 
with  progressive  diminution  in  the  blood  supply  to  the  part  (Halsted). 
The  course  of  the  artery  may  show  patches  of  hardening  with  indentations 
and  widenings,  collar-like  constrictions,  or  uniform  widenings;  or,  on  the 
other  hand,  the  arteries  may  be  converted  into  uniform  tubes  whose  walls 

may  give  the  sensation  of  rubber 
tubes  on  the  one  hand  (uniform 
fibrous  sclerosis),  or  of  absolute 
pipe-stems  (complete  calcification) 
on  the  other.  This  condition  is,  of 
course,  particularly  common  in 
arteriosclerosis  affecting  the  base 
of  the  aorta  and  in  the   arterio- 


FiG.  166. — Sclerosis  of  a  coronary  artery,  producing  an  area  of  infarction  near  the  apex.  A.  Show- 
ing the  entire  specimen.  B.  The  sclerotic  coronary  artery,  camera  brought  closer;  a  wire  has  been  passed 
through  the  mouth  of  the  coronary  artery. 

sclerotic  form  of  aortic  insufficiency,  and  may  account  for  many  of  the 
symptoms  to  be  discussed  later  (see  page  284). 

Since  the  heart  muscle  requires  much  more  blood  when  it  is  beating 
forcibly  and  rapidly  than  when  it  is  beating  slowly  and  quietly,  it  is  easily 
seen  that  this  collateral  circulation  may  be  sometimes  adequate  and  some- 
times not.  Also,  since  in  different  individuals  of  the  same  species  there  are 
variations  both  in  the  structure  and  disposition  of  the  minute  arteries  and 
in  the  needs  of  the  muscle-fibres  for  nourishment,  it  is  but  natural  that  the 
results  of  coronary  disease  should  vary  greatly. 


CLINICAL   MANIFESTATIONS. 


The  clinical  pictures  associated  with  coronary  sclerosis  are  character- 
ized by  some  or  all  of  the  following  features:  pain  over  the  precordium 
or  down  the  arms,  feelings  of  suffocation  or  of  impending  death. 


SCLEROSIS   OF  THE   CORONARY   ARTERIES.  283 

paroxysms  of  most  intense  dyspnoea  with  palpitation,  enlargement 
and  pulsation  of  the  liver,  general  weakness,  sudden  death. 

A  considerable  grade  of  arteriosclerosis  may  be  present  in  both  young 
and  old  individuals  without  giving  any  symptoms  whatever,  as  shown  in 
the  case  of  J.  L.  (page  467).  Another  example  of  this  was  a  colored  boy 
under  the  writer's  care  who  after  very  vigorous  life  died  at  the  age  of  nine- 
teen in  the  fifth  week  of  typhoid  fever.  Neither  before  nor  during  the  fever 
had  he  had  any  cardiac  symptoms.  However,  his  coronary  arteries  were 
found  to  be  very  sclerotic. 

Sudden  Death. — S  udden  death  is  frequently  the  first  manifesta- 
tion of  the  condition,  and  examples  are  almost  daily  in  the  newspapers  of 
persons,  usually  men  past  middle  life,  who  drop  dead  without  warning  and 
with  no  previous  illness,  due  to  sudden  thrombosis  of  the  sclerotic  coro- 
nary arteries,  or  perhaps  merely  to  the  fact  that,  though  the  sclerotic 
process  has  been  going  on  gradu'ally,  the  instant  has  passed  at  which  the 
cardiac  nutrition  becomes  insufficient  and  ischsemia  sets  in  with  sudden 
functional  insufficiency,  just  as  occurs  in  the  leg  in  intermittent  claudica- 
tion. This  must  be  the  case  in  many  hearts  in  which  no  actual  thrombosis 
or  embolism  can  be  found  post  mortem. 

Paroxysms  of  dyspnoea  such  as  those  described  on  page  148,  the  so- 
called  cardiac  asthma,  are  also  extremelj''  common  in  coronary  sclerosis, 
especially  when  combined  with  aortic  insufficiency  (vide  page  366),  in 
which  case  they  are  no  doubt  due  to  the  dilatation  and  weakening  of  the 
left  heart  and  the  consequent  accumulation  of  COj  in  the  blood.  It  has 
been  suggested  by  Drs.  C.  M.  Cooper  and  E.  O.  Jellinek  of  San  Francisco 
that  this  was  always  an  accompaniment  of  sclerosis  of  the  right  coronary 
artery  and  dilatation  of  the  right  heart,  but  in  autopsies  of  two  cases  under 
the  writer's  care  who  had  suffered  from  such  attacks  the  right  coronary 
was  absolutely  free  from  sclerosis. 

Sensations  of  pain  in  the  precordium,  and  especially  behind  the  sternum, 
as  well  as  pains  and  tenderness  over  various  interspaces  and  radiating  down 
the  arms,  are  especially  common  in  coronary  sclerosis. 

Paroxysmal  Tachycardia.  —  Attacks  of  tachycardia  beginning  with 
sudden  doubling  of  the  pulse-rate  and  ending  in  sudden  halving  of  the  latter, 
just  as  is  present  in  essential  paroxysmal  tachycardia,  have  been  described 
by  Romberg  as  manifestations  of  coronary  sclerosis,  and  Krehl  also  cites 
similar  findings. 

In  Romberg's  case  the  pulse- rate  rose  suddenly  from  100  to  200,  while  the  respira- 
tion remained  at  20.  The  attack  lasted  two  days  and  then  the  pulse-rate  dropped  sud- 
denly to  100.  Later  an  aortic  stenosis  developed  gradually  and  the  patient  died  of  heart 
failure,  the  autopsy  showing  aortic  stenosis  and  sclerosis  and  marked  coronary  sclerosis. 
Dr.  Barker  informs  the  writer  that  he  also  has  seen  a  couple  of  cases  in  which  such 
attacks  were  associated  with  coronary  sclerosis. 

Quite  recently  similar  attacks  have  been  produced  by  T.  Lewis  upon  ligating  the 
coronary  arteries  in  cats  even  after  the  cardiac  nerves  had  been  sectioned. 

Painful  sensations  about  the  heart  are  particularly  common  in  asso- 
ciation with  coronary  sclerosis,  but  on  the  one  hand  they  are  by  no  means 
confined  to  this  condition,  and  on  the  other  hand  most  extensive  coronary 
sclerosis  may  be  present  without  the  occurrence  of  cardiac  pain.  The  most 
marked  form  of  cardiac  pain,  the  so-called  "angina  pectoris"  (pronounced 


284  DISEASES   OF   THE   HEART   AND    AORTA. 

an'gina,  not  angl'na)  to  be  discussed  below,  is  in  its  most  typical  form 
usually  associated  with  a  certain  degree  of  coronary  sclerosis. 

ANGINA    PECTORIS. 

In  1768  both  Heberden  and  Rougnon  described  attacks  of  pain  in  the 
chest.  Tne  former  recognized  the  condition  the  more  clearly  and  described 
it  in  the  following  words: 

"But  there  is  a  disorder  of  the  breast  marked  with. strong  and  peculiar  symptoms, 
considerable  for  the  kind  of  danger  belonging  to  it,  and  not  extremely  rare,  which  deserves- 
to  be  mentioned  here  at  length.  The  seat  of  it,  and  sense  of  strangling  and  anxiety  with 
which  it  is  attended,  may  make  it  not  improperly  be  called  angina   pectoris. 

"  They  who  are  afflicted  with  it  ai  e  seized  while  they  are  walking  (more  espe- 
cially if  it  be  up-hill  and  soon  after  eating)  with  a  painful  and  most  disagreeable 
sensation  in  the  breast,  which  seems  as  if  it  would  extinguish  life  if  it  were  to  increase  or 
to  continue;  but  the  moment  they  stand  still  all  this  uneasiness  vanishes. 

"In  all  other  respects  the  patients  are,  at  the  beginning  of  the  disorder,  perfectly 
well,  and  in  particular  have  no  shortness  of  breath,  from  which  it  is  totally 
different.  The  pain  is  sometimes  situated  in  the  upper  part,  some- 
times in  the  middle,  sometimes  at  the  bottom  of  the  os  sterni, 
and  often  more  inclined  to  the  left  than  to  the  right  side.  It  like- 
wise very  frequently  extends  from  the  breast  to  the  middle  of  the  arm.  The  pulse  is, 
at  least  sometimes,  not  disturbed  by  this  pain,  as  I  have  had  opportunities  of 
observing  by  feeling  the  pulse  during  the  paroxysm.  Males  are  most  liable  to  this 
disease,  especially  such  as  have  passed  their  fiftieth  year.  After  it  has  con- 
tinued a  year  or  more,  it  will  not  cease  as  instantaneously  upon  standing  still,  and  it  will 
come  on  not  only  when  the  persons  are  walking  but  when  they  are  lying 
down,  especially  if  they  lie  on  the  left  side,  and  oblige  them  to  rise  out  of  their  beds. 
In  some  inveterate  cases  it  has  been  brought  on  by  the  motion  of  a  horse  or  a  carriage 
and  even  by  swallowing,  coughing,  going  to  stool,  speaking,  or 
any   disturbance   of  mind. 

"Such  is  the  usual  appearance  of  this  disease,  but  some  varieties  may  be  met  with. 
Some  have  been  seized  while  they  were  standing  still  or  sitting,  also  upon  first  waking  out 
of  sleep,  and  the  pain  sometimes  reaches  down  the  right  arm  as  well 
as  the  left  and  even  down  to  the  hands,  but  this  is  uncommon;  in  a 
very  few  persons  the  arm  has  at  the  same  time  been  numbed  and  swelled.  In  one  or  two 
persons  the  pain  has  lasted  some  hours  or  even  days,  but  this  has  happened  when  the  com- 
plaint has  been  of  long  standing  and  thoroughly  rooted  in  the  constitution;  once  only  the 
very  first  attack  continued  the  whole  night. 

" I  have  seen  nearly  a  hundred  people  under  this  disorder,  of  which  num- 
ber there  have  been  three  women  and  one  boy  two  years  old.  All  the  rest 
were  men  near  or  past  the  fiftieth  year  of  their  age. 

"  Persons  who  have  persevered  in  walking  till  the  pain  has  returned  four  or  five  times 

have  then  sometimes  vomited The  termination  of  angina  pectoris  is  remarkable. 

For  if  no  accident  intervene  but  the  disease  go  on  to  its  height,  the  patients  all 
suddenly  fall  down  and  perish  almost  immediately.  The  angina 
pectoris,  as  far  as  I  have  been  able  to  investigate,  belongs  to  the  class  of  spasmodics,  not 
of  inflammatory  complaints.     For, 

"In  the  first  place,  the  access  and  the  recess  of  the  fit  is  sudden. 

"Secondly,  there  are  long  intervals  of  perfect  health. 

"Thirdly,  wine  and  spirituous  liquors  and  opium  afford  considerable  relief. 

"Fourthly,  it  is  increased  by  disturbance  of  mind. 

"Fifthly,  it  continues  many  years  without  any  other  injury  to  the  health. 

"Sixthly,  in  the  beginning  it  is  not  brought  on  by  riding  on  horseback  or  in  a  car- 
riage, as  is  usual  in  diseases  arising  from  scirrhus  or  inflammation. 

"Seventhly,  during  the  fit  the  pulse  is  not  quickened. 

"Lastly,  its  attacks  are  often  after  the  first  sleep,  which  is  a  circumstance  common 
to  many  spasmodic  disorders. 


ANGINA   PECTORIS.  285 

"With  respect  to  the  treatment  of  this  complaint,  I  have  little  or  nothing  to  advance. 
.  .  .  .  Quiet,  warmth,  and  spirituous  liquors  help  to  restore  patients 
who  are  nearly  exhausted  and  to  dispel  the  effects  of  a  fit  which  does  not  soon  go  off. 
Opium   taken  at  bedtime  will  prevent  the  attacks  at  night." 

Heberden's  contemporary,  the  great  John  Hunter,  suffered  from  this 
disease,  and  described  his  attacks  most  vividly. 

The  modern  aspects  of  the  whole  subject  have  been  discussed  in  a 
masterly  way  by  Sir  W.  Gairdner  as  well  as  in  the  more  recent  monographs 
of  W.  Osier  and  G.  A.  Gibson. 

CHARACTER    OF    THE    PRECORDIAL    PAIN    AND    CLINICAL    SUMMARY. 

In  Heberden's  description  we  have  epitomized  almost  all  the  clinical 
features.  (1)  The  sudden  attacks  of  oppression  in  the  chest,  with  a  feeling 
of  strangling,  and,  as  Hunter  puts  it,  "as  though  the  sternum  was  being 
drawn  back  to  the  spine,"  or,  in  the  words  of  Matthew  Arnold,  as  "though 
there  were  a  mountain  upon  my  chest."  (2)  The  mental  anguish  (termed 
by  Gairdner  angor  animi) ,  with  the  fear  of  impending  death,  especially  pro- 
nounced in  John  Hunter.  (3)  The  intense  pain,  situated  sometimes  in  the 
lower  sometimes  in  upper  part  of  the  sternum,  more  frequently  to  the  left 
than  to  the  right  (although  occasionally  to  the  latter),  and  very  often 
radiating  to  the  arm,  especially  the  left.  (4)  Some  of  the  disturbances 
of  sensation;  even  Heberden  speaks  of  numbness  of  the  arm.  (5)  Changes 
in  the  pulse  in  some  cases:  intermissions;  extrasystoles  in  some  cases 
(Hunter) ;  alternating  pulse  in  others  (Mackenzie) .  (6)  The  extreme  pallor 
and  constriction  of  peripheral  arteries  during  the  attack.  (7)  The  sudden 
death.  (8)  The  main  factors  in  bringing  on  attacks, — walking  up-hill, 
flatulence  and  digestive  disorders,  bending  down  in  undressing,  mental 
excitement  or  anxiety,  and  especially  anger;  but  none  of  the  more  gentle 
emotions,  such  as  pity,  sorrow,  etc.,  even  when  felt  intensely.  (The  effect 
of  exposure  to  cold  does  not  seem  to  be  mentioned  by  these  writers.)  (9) 
The  association  of  the  condition  with  sclerosis  of  the  coronary  arteries.  (10) 
Its  frequent  association  with  abnormal  fatty  deposits  about  the  heart 
(cf.  Jenner  and  also  page  214).  (11)  The  relief  of  symptoms  by  means  of 
opium,  warm  applications,  hot  drinks  (vasodilator  mechanisms),  and 
counter-irritation  (Heberden).  (12)  Its  incurability,  owing  to  the  seat  of 
the  trouble. 

To  these  points  clinical  observations  since  Jenner  have  added:  (1) 
The  existence  of  anginoid  attacks  with  several  conditions  other  than  those 
of  coronary  sclerosis,  particularly  with  over-indulgence  in  tobacco,  with 
hysteria,  with  hyperthyroidism,  and  with  other  purely  vasomotor  phe- 
nomena, as  well  as  with  practically  all  the  valvular  diseases  of  the  heart. 
(2)  The  frequent  association  of  angina  pectoris  with  certain  definite  areas 
of  tenderness  which  represent  spinal  segments  corresponding  to  the  referred 
pain.  (3)  The  occurrence  of  rise  in  blood-pressure  with  each  attack.  (4) 
The  relief  of  the  attacks  by  inhalations  of  amyl  nitrite  and  other  vasodilator 
drugs. 

Sir  William  Gairdner  has  called  attention  to  the  occurrence  of  certain 
cases  resembling  Heberden's  angina  pectoris  in  every  way  except  in  the 
absence  of  pain  as  a  symptom  (angina  sine  dolore) . 


286 


DISEASES   OF   THE   HEART   AND    AORTA. 


Paths  Traversed  by  the  Pain  Sensations. — The  afferent  impulses  from 
the  heart  have  been  traced  by  Ludwig  and  Cyon  through  the  depressor 
fibres  of  the  vagus.  It  has  been  shown  by  Eyster  and  Hooker  that  the 
afferent  impulses  from  the  aorta  and  coronary  arteries  do  not  take  this 
same  path  but  pass  upward  in  the  main  bundle  of  the  vagus.  There  is  no 
evidence  from  animal  experiment  that  afferent  impulses  pass  in  any  other 
way;  but  Henry  Head,  as  a  result  of  his  most  extensive  studies  upon  pain 
in  visceral  disease,  states  that  this  "  produces  impulses  which  pass  into 
the  spinal  cord  by  the  white  rami.  The  segment  on  which  they 
infringe  is  excited  and  pain  is  produced.  At  the  same  time  all  potentially 
painful  influences  passing  into  this  segment  from  the  afferent  nerves  are 
exaggerated,  and  ultimately  the  body  wall  may  become  tender." 

These  sensations  of  referred  pain  follow  the  same  path  as  has  been  described  by 
Bayliss  for  the  vasodilator  fibres  with  which  protopathic  sensation  seems  to  be  closely 
associated,  as  shown  in  herpes  zoster,  etc.  Protopathic  sensations  are  referred  back  to  the 
distribution  of  the  corresponding  nerve  segments  without  close  reference  to  the  points 
at  which  they  arise. 

Insensibility  of  the  Heart  to  Touch. — The  heart  itself  seems  to  be  devoid  of  tactile 
sensation,  for  Harvey  gives  the  following  description  of  the  condition  in  the  nineteen-year- 
old  son  of  Viscount  Montgomery,  who  had  a  fistulous  opening  in  the  chest  wall  over  the 
heart  following  fracture  of  the  rib  in  early  childhood.    "  I  found  a  large  open  space  in  the 

chest  into  which  I  could  introduce  three  of  my 
fingers  and  my  thumb  ...  I  saw  that  I  was 
handling  the  apex  of  the  heart !  covered  over  with 
a  layer  of  fungous  flesh  by  way  of  external  de- 
fence, as  commonly  happens  in  old  foul  ulcers. 
.  .  .  The  youth  never  knew  when  we  touched 
his  heart  except  by  the  sight  or  the  sensation  he 
had  through  the  external  integument." 

Palpitation  and  Anginal  Sensations 
Compared. — The  sensations  which  may  be 
felt  from  the  heart  itself  may  be  either 
rhythmic  and  felt  as  a  distinct  sensation 
accompanying  each  systole  of  the  heart, 
such  as  the  feelmg  of  palpitation,  or  the 
pain  felt  at  each  beat  in  some  cases  of 
pericarditis,  especially  those  associated 
with  pneumonia.  The  sensation  in  the 
latter  condition  may,  however,  arise  in 
the  parietal  pericardium,  and  may  have 
nothing  to  do  with  the  heart  itself. 

Sensations  of  palpitation  may  be 
very  distressing,  partly  on  account  of  the 
feelings  of  suffocation  which  accompany 
them,  partly  on  account  of  the  mechan- 
ical shock  of  the  heart  beating  forcibly  against  the  chest  wall  like  a  bird 
in  a  cage.  But,  however  intense  and  distressing,  the  sensation  of  palpi- 
tation is  always  a  pressure  sensation  and  never  one  of  pain.  On  the  other 
hand,  the  real  cardiac  pain  is  never  intermittent,  never  felt  as  a  distinct 
sensation  with  each  beat  of  the  heart,  but,  whether  dull  and  aching  or 
sharp  and  stabbing,  it  has  no  throbbing  quality  about  it.    It  is,  therefore, 


Fig.  167. — Distribution  of  pain  in  attacks 
of  angina  pectoris.  (Schematic,  after  Head 
and  Mackenzie.)  ASCAO,  area  correspond- 
ing to  the  ascending  aorta;  TR,AO,  area  cor- 
responding to  the  transverse  aorta;  L.A,R.A, 
area  corresponding  to  left  and  right  auricles. 


ANGINA   PECTORIS. 


287 


not  at  all  homologous  with  the  sensation  of  palpitation  and  must  belong 
to  a  quite  different  category.  Hirschfelder  has  added  some  evidence  for 
this  view  by  observing  that  in  some  cases  of  palpitation  the  sensation 
was  referred  definitely  to  the  root  of  the  aorta,  and  was  exactly  similar 
in  character  to  other  sensations  of  throbbing  in  the  radial  artery  alone, 
which  were  sharply  localized  along  its  course  and  not  spreading  like  a  pro- 
topathic  sensation. 

Referred  Pains  in  Angina  Pectoris. — James  Mackenzie  and  Henry 
Head  have  called  attention  to  the  commonness  of  referred  pain  and  tender- 
ness in  angina  pectoris.  Mackenzie  showed  that  there  is  often  tenderness 
in  the  areas  supplied  by  the  second 
and  third  cervical  segments,  whose 
fibres  along  with  some  from  the 
spinal  accessory  run  down  to  the 
heart  through  the  vagus.  This  would 
account  for  the  occipital  headaches 
and  tenderness  of  the  sternocleido- 
mastoid and  trapezius  muscles  which 
are  frequently  present.  The  muscu- 
lar tenderness  is  elicited  by  squeez- 
ing gently  between  the  thumb  and 
forefinger. 

The  distribution  of  the  pain  and 
hyperesthesia,  according   to    Head, 
bears  a  close  relation  to  the  chamber  most  affected,  and  particularly  to 
the  somatic  segment  of  the  embryo  to  which  it  corresponds. 


Fig.  168. — Distribution  of  attacks  of  pain  and 
sensory  disturbances  in  a  case  of  angina  pectoris. 
(After  Head,  with  permission  of  the  pubhshers  of 
Brain.) 


Correspond  embryo- 
logically  to 

Nerve  .supply 

Associated  phenomena  and 
pain  referred  to 

Auricles 

5,  6,  7,  8  thoracic 
2,3,4,5,6  thoracic 

5,  6,  7,  8  segments 

2-6  thoracic  seg- 
ments 

Lower    axilla    and    shoulder- 

Ventricles 

blades. 
Chest   wall   from   2d-7th  rib, 
ulnar    surface    of    forearm 
to  wrist,   and  inner  aspect 

Ascending  aorta.  .  . 
Transverse  arch .  .  . 

3  and  4  cervical.  . 
C.  IV 

3   and   4  cervical 
segments 

C.  IV 

of  upper  arm. 

These  segments  also  to  3  and  4 
c.  and  1  thor.  Tenderness 
in  neck  of  sternomastoid  and 
trapezius  muscles.  Tender- 
ness and  pain  at  back  of 
neck.   (Dilatation  of  pupil?) 

Laryngeal  areas  of  neck  (4th 
branchial  bar). 

Back  or  front  of  chest,  espe- 
cially below  nipple;  abdo- 
men. 

Outer  two-thirds  of   arm  and 

Descending  aorta.  . 
Pulmonary  artery. 

Thoracic  segments 
corresponding 
2-12 

C.V-VIII 

2-12,  esp.  4-12... 
C.  V 

hand;    arm  muscles. 

Thus,  the  auricles  (atria),  which  are  the  hindmost  in  the  development  of  the  cardiac 
tube,  receive  their  innervation  from  and  refer  their  pain  to  the  fifth,  sixth,  seventh,  and 
eighth  thoracic  segments.     The  ventricles,  the  next  chambers  headward,  correspond  to 


288 


DISEASES   OF   THE    HEART   AND    AORTA. 


the  second  to  the  sixth  thoracic;  the  ascending  aorta  from  the  semilunar  valves  to  the 
origin  of  the  ductus  arteriosus  corresponds  to  the  primitive  aorta  with  the  third  and  fourth 
branchial  artery,  and  the  pain  is  referred  to  these  segments  (but  an  aneurism,  etc.,  involv- 
ing this  in  adult  Hfe  will  also  involve  the  neighboring  nerves  and  the  pain  will  be  referred 
to  the  first,  second,  and  third  thoracic  segments  as  well).  The  fifth  to  the  eighth  cervical 
segments,  corresponding  to  the  pulmonary  artery,  will  not  be  involved,  and  pain  may  not 
be  referred  over  these  areas.'  (There  are  many  notable  exceptions  to  this  rule  even  among 
Head's  cases;   but  there  is  usually  overlapping  of  these  areas.) 

Sudden  Death  and  Motor  Disturbances. — The  phenomena  thus  far 
considered  are  purely  sensory;  and  the  question  arises,  what  are,  if  an}', 
the  motor  disturbances  connected  with  angina  pectoris?  It  is  evident  that 
the  cessation  of  the  heart-beat  in  sudden  death  that  occasionally  occurs 

may  be  due  either  to  the  occlusion 
of  the  artery  or  to  a  sudden  onset 
of  complete  heart-block  as  in  the 
Adams-Stokes  syndrome.  The  lat- 
ter condition  is  sometimes  associ- 
ated with  angina  pectoris  and  verj^ 
frequently  with  coronary  sclerosis 
(see  page  472),  though  this  is  rare, 
and  more  frequently  the  pulse  be- 
comes regular  after  a  short  time,  or 
sudden  death  from  heart-failure  sets 
in  just  as  in  the  experiments  of  Cohn- 
heim  and  v.  Schulthess-Rechberg. 

During  the  attacks  of  angina 
pectoris  the  blood-pressure  is  often 
high,  though  Mackenzie  states  that  in  many  cases  there  is  no  change 
whatever.  This  seems  to  be  due  to  a  true  pectoral  vasomotor  crisis  in  the 
sense  of  Pal,  rising  sharply  with  and  falling  sharply  after  the  attack,  as 
shown  in  Fig.  169. 


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Fig.  169. — Blood-pressure  curve  showing  crises  of 
hypertension  during  attacks  of  angina  pectoris. 


ETIOLOGY    AND    VARIETIES    OF    ANGINA    PECTORIS. 

The  idea  that  sclerosis  of  the  coronary  arteries  was  the  lesion  which 
caused  angina  pectoris  seems  to  have  originated  not  with  Heberden  but 
with  Edward  Jenner,  the  discoverer  of  vaccination,  who  was  so  certain  of 
its  pathology  that  before  doing  an  autopsy  upon  a  case  he  made  a  bet 
with  a  friend  that  he  would  find  thickening  of  the  coronary  arteries.  He 
won  the  bet. 

This  indeed  seems  to  be  correct  for  almost  all  cases  of  fatal  angina, 
since  Huchard  found  coronary  sclerosis  present  in  128  out  of  145  autopsies 
recorded  in  the  literature,  and  most  of  the  others  were  in  cases  of  adherent 
pericardium  or  valvular  disease.  A  few  cases  of  death  have  occurred  in 
attacks  of  angina  due  to  tobacco  or  in  post-febrile  conditions  where  the 
coronary  arteries  were  clear,  but  in  these  the  possibility  of  obscure  myo- 
cardial change  must  be  borne  in  mind  (Osier). 


'  His  own  cases  56,  57,  and  58,  as  well  as  cases  of  many  other  writers,  show  tenderness 
during  and  after  attacks  due  to  aneurism  involving  the  ascending  aorta. 


ANGINA   PECTORIS.  289 

Angina  Pectoris  without  Coronary  Sclerosis. — However,  in  1812,  J. 
Latham  reported  a  number  of  cases  which,  in  spite  of  the  occurrence  of 
intense  anginal  symptoms,  did  not  run  the  usual  course  ending  in  sudden 
death,  and  to  these  he  gave  the  name  of  "pseudo-angina"  (angina 
notha) . 

Bean,  Stokes,  and  Graves  also  described  reflex  and  toxic  forms  of 
angina,  but  a  much  clearer  light  was  thrown  upon  the  subject  by  Noth- 
nagel's  article  entitled  "Angina  pectoris  vasomotoria."  He  says,  "We 
must  interpret  this  sj'mptom-complex  to  indicate  that  we  are  not  dealing 
with  a  disease  which  arises  primarily  in  the  heart,  but  that  the  symptoms 
of  stenocardia  are  of  secondary  origin  and  are  brought  on  by  a  very  general 
spasm  of  the  arteries." 

The  term  "pseudo-angina"  has  been  severely  criticised  by  Balfour 
and  Gibson,  since  "angina"  is  a  symptom,  not  a  disease,  and  in  all  cases  it 
is  a  very  real  one.  Nothnagel's  term,  "vasomotor  angina,"  or  Huchard's 
"reflex  angina,"  seems  to  the  writer  to  be  preferable. 

Theories  as  to  Causation  of  Anginal  Pain. — Many  theories  have  been 
advanced  to  explain  the  causation  of  pain  in  anginal  attacks.  These  may 
be  classified  as  follows: 

(1)  Ischaemia  '.om  Coronary  Stenosis. — The  original  view  of  Jenner  was  later  supple- 
mented by  Allan  Burns,  that  the  attack  may  be  brought  on  by  asphyxia  of  the  heart  muscle 
when  there  was  a  disproportion  between  the  amount  of  blood  flowing  to  it  and  the  amoimt 
of  blood  which  it  needed.  Potain,  in  1870,  was  the  first  to  introduce  the  theory  that 
angina  pectoris  is  due  to  "the  intermittent  claudication  of  the  heart";  but  Allan  Bums 
had  already  completely  demonstrated  this  causal  factor  in  1809  and  had  described  his 
observations  in  the  following  words:  "If  we  call  into  vigorous  action  a  limb  round  which 
we  have  with  a  moderate  degree  of  tightness  applied  a  ligature,  we  find  that  the  member 
can  only  support  its  action  for  a  very  short  time,  for  now  its  supply  of  energy  and  its  expen- 
diture do  not  balance  each  other  ...  we  witness  an  induction  of  an  extreme  degree 
of  debility  and  we  have  the  patient  complaining  of  an  unusual  painful  feeling  in  the  hmb, 
but  still  all  its  muscles  are  in  a  state  of  inactivity.  .  .  .  If  a  person  with  the  arteries 
of  the  heart  diseased  in  such  a  way  as  to  impede  the  progress  of  the  blood  along  them 
attempt  to  do  the  same  (ascend  a  steep  or  mount  a  pair  of  stairs),  he  finds  that  the  heart 
is  sooner  fatigued  than  the  other  parts  are,"  and  the  same  pain  results. 

(2)  Ischaemia  from  vasoconstrictor  spasm  of  the  coronary  arteries,  which  reduces 
the  functional  condition  to  the  same  state  as  described  by  Allan  Burns  for  the  coronary 
sclerosis.  This  seems  to  apply  to  the  vasomotor  and  toxic  anginas  and  often  consti- 
tutes a  factor  superimposed  upon  the  coronary  sclerosis  in  the  angina  vera.  Such  an 
action  of  drugs  upon  the  coronary  vessels  has  been  demonstrated  on  the  excised  heart  by 
O.  Loeb,  Langendorff,  and  Wiggers  (see  page  281). 

(3)  Acuie  dilatation  of  the  heart,  producing  a  pain  similar  to  that  of  in- 
testinal colic.  This  theory  particularly  has  been  adhered  to  by  many  writers.  The 
similarity  between  the  anginal  pain  and  that  of  renal,  biliary,  pancreatic,  and  intestinal 
colic  suggests  that  it  belongs  to  the  common  form  by  which  the  visceral  nerves  give 
expression  to  overdistention.  Some  dilatation  usually  accompanies  the  attack,  and 
seems  to  be  a  primary  cause  of  the  pain  in  cardiac  overstrain  and  in  many  cases  of  val- 
vular lesion. 

(4)  Neuritis. — It  may  at  times  be  due  to  neuritis  of  the  cardiac  nerves,  or,  on 
the  other  hand,  to  a  neuritis  primary  in  the  brachial  nerves  and  referred  to  the  heart. 
Lesions  of  the  cardiac  plexus  have  been  described  by  Lancereaux,  Grocco,  and  Benenati,  but 
Herard  and  others  have  failed  to  find  them.  Nevertheless  it  is  quite  possible  that  sub- 
stances like  tobacco  (nicotine),  which  stimulate  sensory  nerves  in  the  heart  and  which  have 
a  specially  toxic  action  upon  the  ganglion  cells,  may  produce  toxic  neuritis  of  these  nerves. 

(5)  Neuralgia   of  the  cardiac  nerves. 

(6)  Action  of  other  constitutional  diseases  like  gout,  diabetes,  and  chronic  nephritis. 
19 


290  DISEASES   OF   THE   HEART    AND    AORTA. 

But  it  is  most  probable  that  the  effects  are  due  to  the  other  above-mentioned  factors  which 
accompany  these  diseases, — arteriosclerosis  and  the  presence  of  vasoconstrictor  substances 
either  as  retention  products  or  internal  secretions. 

ASSOCIATED    CLINICAL    CONDITIONS. 

The  various  conditions  with  which  angina  is  associated  most  commonly 
might  be  classified  as  follows: 

I.  Organic  Lesions. 

A.  Sclerosis  of  coronary  arteries. 

B.  Aneurism,  especially  of  first  part  of  ascending  aorta. 

C.  Valvular  lesions,  especially  aortic  insufficiency.    (This  constitutes  a  very 

common  group.) 

D.  Aortic  aneurism,  especially  of  the  sinuses  of  Valsalva  and  the  ascending 

arch. 

E.  Adherent   pericardium.      (The   most   frequent   form   which  is  seen  in 

children.) 
II.  Vasomotor  anginas. 

A.  Hysterical  type,  most  common  in  women,  associated  with  other  vaso- 

motor disturbances  and  stigmata  of  hysteria. 

B.  Toxic,  due  to  the  action  of  various  poisons,  esf)ecially  (a)  tobacco,  (6) 

caffeine,  taken  both  as  tea  and  as  coffee. 

C.  Associated  with  hyperthyrodism  and  exophthalmic  goitre. 

III.  Attacks  of  more  or  less  anginoid  pain  occur  in  the  cases  of  acute  dilatation  of 
healthy  hearts,  due  to  primary  cardiac  overstrain. 

Angina  Pectoris  in  Valvular  Diseases. — The  attacks  of  angina  pectoris 
associated  with  coronary  sclerosis,  which  represent  the  original  form  de- 
scribed by  Heberden,  are  usually  designated  as  angina  vera.  These  are 
very  often  associated  with  valvular  lesions,  especially  with  aortic  insuffi- 
ciency in  which  the  coronary  lesions  are  usually  continuous  with  those  of 
the  aorta,  but  they  are  also  common  in  association  with  other  valvular 
lesions,  since  it  is  rare  to  find  a  case  of  chronic  valvular  disease  without 
some  disease  of  the  coronary  arteries.  The  presence  of  valvular  disease, 
therefore,  rather  favors  than  excludes  the  diagnosis  of  coronary  sclerosis. 

In  spite  of  the  frequency  with  which  these  two  conditions  are  asso- 
ciated, occasionally  one  encounters  cases  of  angina  with  valvular  disease, 
especially  aortic  insufficiency,  without  any  disease  of  the  coronary  vessels 
whatever,  as  was  well  exemplified  by  a  patient  with  a  ruptured  aortic  valve 
who  was  for  five  years  under  observation  at  the  Johns  Hopkins  Hospital, 
During  this  time  he  suffered  from  very  frequent  attacks  of  typical  angina 
pectoris.  He  died  suddenly  while  at  stool.  Autopsy  showed  rupture  of 
aortic  leaflet.  The  coronary  arteries  were  soft  and  the  walls  were  not 
thickened  anywhere. 

Angina  Pectoris  in  Acute  Dilatation. — It  is  possible:  (1)  that  under 
these  conditions  acute  dilatations  of  the  heart,  due  to  momentary  diminu- 
tion in  tone  of  the  heart  muscle,  might  be  the  immediate  cause  of  the  pain, 
which  would  thus  be  of  primary  cardiac  rather  than  vascular  origin.  (2) 
That  in  such  dilatation,  etc.,  centripetal  stimvdi  may  arise  in  the  heart 
which  may  cause  a  general  vasoconstriction.  (This  is  contrary  to  the  usual 
depressor  effect  of  stimuli  arising  in  the  heart,  but  it  is  not  at  all  certain 
that  in  the  presence  of  such  a  pathological  condition  as  angina  pectoris 
the  paths  of  least  resistance  in  the  central  nervous  system  may  not  be  quite 


ANGINA   PECTORIS.  291 

different  from  what  they  are  in  the  normal  individual.)  (3)  Miss  Hyde  in 
Porter's  laboratory  has  shown  that  dilatation  of  the  heart  in  itself  caused 
diminution  in  the  flow  through  the  coronary  arteries,  and  it  is  possible 
that  the  circulation  may  thus  be  diminished  to  a  point  at  which  relative 
ischajmia  of  the  heart  may  set  in  and  cardiac  pains  result. 

Angina  Pectoris  in  Aneurism. — Attacks  of  angina  pectoris  are  very 
common  in  cases  of  aneurism  involving  the  ascending  arch,  and  especially 
in  early  small  aneurisms  near  the  sinuses  of  Valsalva.  This  has  long  been 
known,  but.  is  the  subject  of  an  especially  interesting  article  by  Dr.  Osier 
upon  "Angina  pectoris  as  an  early  symptom  of  aneurism." 

The  anginoid  pains  in  this  condition  are  probably  simply  reflex,  not  the  result  of 
primary  peripheral  vasoconstriction,  cardiac  ischsemia,  etc.,  but  simply  the  occurrence  of 
pain  sensation  arising  in  the  aortic  walls  from  overstretching  of  the  aorta  under  pressure 
heightened  from  any  cause  whatever,  or  from  increased  excursion  of  the  aortic  wall  as  a 
lesult  of  increased  systolic  output,  etc.,  as  is  so  frequently  seen  in  the  abdomen  in  nervous 
women  with  epigastric  pain  due  to  a  throbbing  of  the  abdominal  aorta.  In  the  later  stages 
of  the  aneurism,  the  symptoms  may  be  less  intense,  due  perhaps  to  the  fact  that  by  erosion, 
etc.,  pressure  upon  the  aneurism  has  diminished,  perhaps  to  the  fact  that  after  a  time 
endings  of  the  sensory  nerves  have  been  permanently  injured  or  rendered  less  sensitive 
by  the  progressive  change  in  the  aortic  wall. 

Anginal  Attacks  in  Children. — Angina  pectoris  also  occurs  in  children,  especially  in 
association  with  mitral  stenosis,  as  illustrated  by  the  following  case:  The  patient  was 
a  boy  aged  8  who  had  had  rheumatism  in  the  right  hip  two  years  previously,  and  since 
then  "had  attacks  of  pain  over  the  heart,  especially  after  exercise.  The  pain  was  so 
severe  that  it  compelled  him  to  stand  perfectly  still  until  it  passed  off;  his  cheeks  became 
blue  and  pale.  He  sometimes  felt  as  though  held  in  a  vise,  but  never  had  any  feeling  of 
fear.  He  also  had  at  times  pain  on  the  right  side  over  about  the  sixth  rib,  which  was 
sometimes  present  with  that  on  the  left  side,  but  often  present  without  it.  Exercise  seemed 
to  bring  on  both.  Examination  showed  a  very  shghtly  enlarged  heart  with  systolic  retrac- 
tion over  the  fourth  left  interspace,  none  about  origin  of  diaphragm  (Broadbent's  sign 
absent).  Area  of  cardiac  flatness  changes  with  respiration.  The  first  sound  at  the  apex 
was  snapping  in  character  and  was  preceded  by  a  well-defined  rumble.  Second  sound  was 
clear,  accentuated  over  the  pulmonic  area.  Pulse  92  per  minute,  of  good  volume,  regular 
in  force  and  rhythm." 

Such  attacks  are  quite  definite  angina  vera  in  the  sense  of  Heberden,  and  indeed  the 
latter  includes  a  similar  case  in  his  list.  In  children  the  association  is,  however,  much 
more  commonly  with  valvular  lesions  than  with  coronary  sclerosis,  and  perhaps  most 
frequently  of  all  with 

Adherent  Pericardium. — This  is  an  extremely  common  concomitant  and  cause  of 
anginal  attacks,  especially  in  children  and  adolescents.  The  pains  are,  perhaps,  simply 
reflex  aches  from  the  ordinary  tugs  upon  the  pericardium,  perhaps  brought  about  by  the 
stretching  of  the  pericardial  fibres  which  occurs  when  the  heart  becomes  dilated. 

VASOMOTOR    ANGINA. 

The  second  great  group  of  cases  with  anginal  symptoms  are  those  in 
which  the  anginal  symptoms  are  of  purely  vasomotor  origin  (Raynaud's 
disease  of  the  heart)  and  are  not  associated  with  organic  lesions, — the 
angina  pectoris  vasomotoria  of  Nothnagel  (angina  pectoris  spuria  of  Latham, 
angines  de  poitrine  reflexes  of  Huchard).  The  characteristic  phenomenon 
in  this  group  is  the  occurrence  of  general  or  local  vasocon- 
striction ushering  in  the  attack;  that  is,  there  are  usually 
coldness,  numbness,  often  tingling,  weakness,  and  heaviness  in  the  left 
arm,  pallor  of  the  latter,  with  marked  diminution  in  size  and  caliber  of 
the  left  radial,  often  also  of  the  right  radial  artery,  sometimes  of  the  vessels 


292  DISEASES   OF   THE   HEART   AND   AORTA. 

of  the  leg,  trunk,  and  head.  The  patient  may  become  pale  and  blue  or  the 
lips  ashen,  and  the  course  of  the  attacks  may  exactly  simulate  those  of 
coronary  sclerosis.  Death  in  such  attacks  is,  however,  extremely  rare. 
It  has  occurred  in  several  cases  in  which  no  coronary  sclerosis  nor  other 
lesion  was  present  to  account  for  the  death.  However,  Dr.  Osier  suggests 
that  in  these  cases  there  may  have  been  myocardial  changes  demonstrable 
only  by  the  method  of  Krehl. 

Hysterical  Angina. — The  most  common  form  of  vasomotor  angina  is 
the  neurotic  or  hysterical  tj'pe,  which  is  most  common  in  young  women 
and  is  associated  with  the  other  stigmata  of  hysteria, — exaggerated  emo- 
tional response  with  marked  histrionic  tendencies,  transitory  vasomotor 
disturbances,  shifting  areas  of  anaesthesia  and  hyperaesthesia,  characteristic 
epileptiform  seizures,  and  the  existence  of  hysteriogenic  zones  where  pres- 
sure calls  forth  the  above-mentioned  symptoms. 

Clinical  Groups  with  Anginal  Symptoms  and  their  Characteristic  Features 

{modified  from,  Huchard) . 

Coronary  Angina. — Site  of  disturbance. — Stenosis  or  obliteration  of  the 
coronary  arteries.  (In  some  cases  valvular  lesion  or  aneurism  only).  Age. 
— Age  of  arteriosclerosis  after  40.  Factors  bringing  on  attack. — Effort  of 
some  sort,  mental  or  physical.  Rarely  spontaneous,  sometimes  nocturnal. 
Not  associated  with  any  other  form  of  neurosis.  Nature  of  pain. — Ag- 
onizing sensation  of  pressure.  Usually  felt  most  acutely  behind  sternum. 
Referred  pain  down  arm,  especially  left  arm,  and  over  chest,  neck,  etc. 
Duration. — 2  to  15  minutes,  stopping  soon  after  standing  still.  Attitude. 
— Silent,  immobile.  Prognosis. — Grave;  almost  always  fatal.  Treatment. 
— Vasodilators. 

Hysterical  Angina. — Site  of  disturbance. — Central  nervous  system  acting 
through  the  vasomotor  nerve  and  cardiac  plexus.  Age. — At  all  ages,  even 
childhood;  sometimes  at  menopause.  Most  frequent  in  women.  Factors 
bringing  on  attack. — Usually  spontaneous  onset  without  effort,  often  recur- 
ring at  fixed  hours  and  associated  with  other  neurotic  symptoms.  Nature 
of  pain. — Pain  less  agonizing,  with  feeling  that  the  heart  is  distended — felt 
most  intensely  at  the  apex.  Duration. — 1  to  2  hours,  not  diminished  by 
standing  still,  not  increased  by  v/alking.  Attitude. — Agitated ;  walking  about. 
Prognosis. — Mild ;  never  fatal.  Treatment. — Antineurotics  and  antineuralgics. 

Qastro-intestinal. — Site  of  disturbance. — Distention  or  neuralgia  due  to 
gastric  troubles.  Age. — At  all  ages,  especially  among  women.  Factors 
bringing  on  attack. — Not  brought  on  by  effort.  Nature  of  pain. — Precordial, 
not  substernal  pain;  with  fulness  of  chest  and  distention  of  heart  but  less 
radiation.  Signs  of  dilatation  of  right  heart;  increase  of  inverse  diameter 
to  right.  Duration. — 1  to  2  hours.  Prognosis. — Death  rare.  Treatment. — 
Antidyspeptic  remedies. 

Tobacco. — Site  of  disturbance. — Spasm  of  coronary  arteries.  Factors 
bringing  on  attack. — Angina  associated  with  toxic  disturbances,  vertigo, 
gastric  and  respiratory  troubles.  Onset  spontaneous.  Nature  of  pain. — 
Attacks  associated  with  bradycardia,  intermittent  pulse,  arrhythmia,  pal- 
pitations.    Attacks  longer  than  those  of  angina  vera.     Prognosis. — Death 


ANGIXA   PECTORIS.  293 

rare.  Attacks  often  disappear  rapidly  on  giving  up  tobacco.  Treatment. — 
Stopping  tobacco,  tea,  and  coffee.  Rest  and  mental  quiet.  Light  diet. 
(Anginas  due  to  tea,  coffee,  etc.,  brought  about  by  the  same  cause.) 

Acute  Cardiac  Overstrain  (with  or  without  Valvular). — Site  of  disturbance. 
— Sudden  dilatation  of  the  heart.  Age. — At  any  age,  but  most  common  in 
young  athletes,  soldiers,  anaemic  girls.  Factors  bringing  on  attack. — Comes 
on  in  the  midst  of  some  unusual  effort,  such  as  a  mountain  climb,  boat  race, 
a  charge,  or  a  dance.  Nature  of  pain. — In  the  heart  itself,  usually  retro- 
sternal. Associated  with  signs  of  dilatation  to  right  and  left,  extreme 
dyspnoea,  often  systolic  murmur  and  arrhythmia.  Duration. — In  maxi- 
mum intensity  a  few  minutes,  after  cessation  of  attack,  the  pains  often 
continuing  or  recurring  as  less  intense  pain,  tachycardia  or  arrhythmia 
usually  persisting  some  time  after  attack.  Attitude. — Immobile.  May 
throw  himself  to  the  ground  in  the  midst  of  the  effort.  Prognosis. — Death 
rare.  Permanent  weakening  of  the  heart  if  the  over-exertion  is  soon  and 
frequently  repeated.  Treatment. — Prolonged  rest  and  general  cardiac 
therapy  until  cardiac  dilatation  has  passed  off;  gradual  resumption  of 
active  life. 

Angina  Pectoris  in  Hyperthyroidism.  —  Very  closely  resembling  the 
neurotic  group  are  the  cases  of  angina  associated  with  exophthalmic  goitre, 
in  which  the  attacks  are  sometimes  more  like  those  of  neurotic,  sometimes 
more  like  those  of  the  coronary  type.  The  crucial  point  in  the  diagnosis 
is  the  detection  of  hyperthyroidism  by  the  application  of  the  numerous 
tests  for  Graves's  disease,  etc. 

A  case  w^hich  has  been  for  the  past  year  and  a  half  and  still  is  under 
the  writer's  care  will  serve  as  type  of  this  condition  (see  page  586). 

Treatment  is  the  same  as  for  the  Graves's  disease  which  is  the  primary 
condition  (see  Part  IV,  Chapter  II).  The  attacks  themselves  may  be 
treated  symptomatically  with  amyl  nitrite,  etc.,  but  the  important  factor 
is  the  treatment  of  the  underlying  disease. 

Tobacco  Angina. — Anginal  attacks  due  to  tobacco  are  not  uncommon, 
both  in  young  persons  beginning  their  first  excesses  in  tobacco  and  in  older 
persons  whose  over-indulgence  is  adding  itself  to  a  beginning  or  advancing 
coronary  sclerosis.  In  both  the  symptoms  disappear  soon  after  the  tobacco 
is  absolutely  given  up,  persistence  of  the  attacks  more  than  a  few  days 
after  this  being  evidence  that  some  damage  to  the  coronaries  has  occurred. 
The  attacks  themselves  may  very  closely  resemble  those  of  true  angina,  but 
very  frequently  precordial  pains  not  of  an  anginal  character  may  be  felt 
by  smokers  between  or  for  some  time  before  such  attacks. 

The  main  factor  in  the  effect  of  tobacco  smoke,  as  shown  by  Ratner  and  Lee,  is  the 
nicotine,  although  small  amounts  of  HCN,  CO,  and  pyridine  bases  are  present  in  the 
smoke.  Moreover,  it  is  probable  that  the  action  of  smoked  tobacco  is  exerted  especially 
upon  the  coronary  arteries,  because  it  enters  the  heart  directly  from  the  pulmonary  vein 
without  prehminary  dilution  in  the  peripheral  circulation. 

Nicotine  seems  to  have  the  effect  of  (1)  stimulating  the  vagus,  (2)  producing  vaso- 
constriction, (3)  thereby  of  raising  the  blood-pressure.  In  most  cases  tliis  leads  gradually 
to  hypertrophy  of  the  heart,  but  in  some,  especially  weaker  individuals,  it  tends  to  facili- 
tate dilatation,  thus  facilitating  angina.  Moreover,  Jackson  and  Matthews  have  recently 
shown  for  aconite,  which  in  many  ways  is  a  similar  drug,  that  much  of  its  action  is  exerted 
through  stimulation  of  the  sensory  endings  of  the  depressor  nerve.  It  is  possible  that  nico- 
tine angina  is  due  in  part  to  similar  sensory  stimulation. 


294  DISEASES   OF   THE   HEART    AND    AORTA. 

Angina  in  Acute  Dilatation. — The  attacks  of  pain  and  precordial  dis- 
comfort during  acute  cardiac  overstrain  and  dilatation  may  reach  anginoid 
intensity,  as  was  noted  by  da  Costa  among  the  soldiers  of  the  Civil  War. 
He  not  infrequently  encountered  patients  who  had  suffered  so  intensely  in 
the  midst  of  a  charge  that  they  could  endure  it  no  longer  and  had  thrown 
themselves  to  the  ground,  exposed  to  almost  certain  death  from  the  point- 
blank  fire  of  the  enemy,  rather  than  continue  to  bear  the  torment  within 
(page  124).  These  pains  are  usually  retrosternal,  often  with  numbness  of 
the  arms  and  tingling  in  the  fingers,  and  associated  with  feeling  of  compres- 
sion and  with  palpitation.  Although  they  occur  in  the  midst  of  extreme 
effort  and  would  scarcely  be  confounded  with  angina  pectoris  vera,  yet, 
since  angina  pectoris  is  a  symptom  and  not  a  disease,  these  cases  must  be 
classed  along  with  it. 

DIAGNOSIS. 

The  actual  differentiation  of  the  various  groups  is  not  always  easy  in 
the  individual  cases,  as  one  frequently  has  a  coronarj'  sclerosis  with  a 
tobacco  angina  superinduced  upon  it,  a  gastric  etiology  where  there  are 
already  attacks  of  angina  vera,  etc.,  and  since  it  is  a  safe  rule  never  to  diag- 
nose the  milder  conditions  until  the  more  serious  can  be  ruled  out  with 
reasonable  probability.  These  cases  may  cause  the  physician  anxiety, 
since  he  remains  uncertain  whether  to  expect  sudden  death  or  whether 
he  is  dealing  with  a  comparatively  mild  condition. 

Case  Illustrating  Doubtful  Diagnosis. 

E.  W.,  widow,  aged  65,  has  had,  since  her  menopause  at  54,  occasional  attacks  of 
precordial  pain,  most  intense  just  behind  the  sternum  and  especially  about  the  level 
of  the  third  costal  cartilage.  She  feels  as  though  some  one  were  bor- 
ing through  from  sternum  to  spine  with  a  sharp  instrument.  The  pain  is 
also  felt  over  the  left  side  of  the  chest  and  down  the  left  arm,  which  sometimes 
becomes  numb,  cold,  weak,  and  heavy.  During  the  attack  she  feels  as  "though  the 
end  has  come."  These  attacks  come  on  apparently  spontaneously  without  definite  asso- 
ciation with  either  emotional  disturbance,  exposure  to  cold,  or  muscular  effort.  They 
last  an  hour  or  two  and  are  relieved  by  amyl  nitrite  or  nitroglycerin.  She  feels 
weak  for  a  day  or  so  after  an  attack,  but  at  other  times  is  extremely  active  for  her  age 
and  rarely  short  of  breath.  The  patient  is  not  at  all  neurotic.  She  has  used  coflfee  and 
beer  in  moderation  all  her  life.  It  must  be  added  that  near  the  end  of  the  menopause 
and  before  the  first  cardiac  attack,  slie  had  a  severe  spell  of  grippe  which  kept  her 
in  bed  for  four  weeks  and  left  her  very  much  prostrated. 

On  physical  examination  the  patient  is  well  nourished.  Slightly  emphysematous, 
but  lungs  otherwise  normal.  Heart  not  enlarged;  action  regular  in  force  and  rhythm; 
sounds  clear,  neither  second  sound  especially  accentuated.  Pulse  between  attacks  is  of 
good  large  volume  and  qiiahty,  apparently  about  normal  tension;  vessel  wall  not  specially 
thickened.  No  ascites.  Liver  not  enlarged.  Feet  always  swollen  from  varicose  veins, 
not  especially  so  during  or  after  attacks. 

In  this  case  the  question  of  crucial  importance  is  whether 
the  angina  is  due  to  the  occurrence  of  the  menopause  and  is 
neurotic,  or  to  the  influenza  which  she  contracted  about  the 
same  time  and  which  may  have  brought  on  a  coronary  sclerosis. 
The  attacks  themselves  resemble  angina  vera,  although  their  duration  is  longer  than 
usual.  The  age  of  the  patient  and  the  history  of  severe  influenza  also  are  in  favor  of  coro- 
nary sclerosis.  On  the  other  hand,  the  fact  that  ordinary  exertion  does  not  seem  to  bring 
them  on,  but  that  they  occur  when  the  patient  is  moderately  quiet,  is  in  favor  of  the  neu- 
rotic.    It  must,  however,  be  borne  in  mind  that  the  patient's  statements  in  this  regard 


ANGINA   PECTORIS.  295 

may  be  inaccurate,  and,  further,  that  in  occasional  cases,  where  the  diagnosis  of  functional 
angina  seemed  quite  well  established,  autopsy  has  shown  definite  coronary  sclerosis. 
It  seems  impossible  to  estabUsh  a  definite  diagnosis  here,  and  the  management  of  the  case 
is  therefore  directed  toward  the  severer  form,  ordering  as  quiet  a  life  as  the  patient  will 
carry  out  (since  potassium  iodide  is  not  well  borne),  vigorous  use  of  amyl  nitrite  and 
nitroglycerin  at  the  time  of  the  attacks,  and  erythrol  tetranitrate  thereafter.  A  diet 
of  small  quantities  of  food  low  in  purin  bodies  and  salt  is  insisted  on. 

Since  these  measures  have  been  instituted  she  has  remained  entirely  free  from 
anginal  attacks  for  over  two  years,  in  spite  of  another  attack  of  influenza.  These  facts 
are  in  favor  of  a  reflex  origin  of  the  condition. 

Differentiation  from  Abdominal  Diseases. — Angina  pectoris  is,  as  a 
rule,  easily  differentiated  from  other  diseases,  though  occasionally  an  attack 
of  biliary,  pancreatic,  or  left  renal  colic  referred  to  the  shoulders  or  even 
intestinal  colic  high  in  the  epigastrium  may  closely  simulate  it.  Careful 
physical  examination  and  location  of  the  areas  of  tenderness  over  the  af- 
fected viscus  should  rule  out  this  error. 

TREATMENT. 

General  Therapeutic  Measures.  —  The  old  treatment  of  Heberden  men- 
tioned above, — "quiet,  warmth,"  and  hot  drinks,  even  if  spir- 
ituous, also  "opium,"  best  in  the  form  of  morphine,  15  mg.  (\  gr.)  hypo- 
dermically  or  by  the  mouth,  during  the  attack,  and  repeated  if  necessary. 
As  Heberden  stated,  it  is  well  to  bring  on  perspiration  (and  hence  vasodila- 
tation) in  any  way  possible.' 

Nitrites.  —  The  most  important  means  for  the  relief  of  the  attack  is, 
however,  the  inhalation  of  amyl   nitrite. 

In  1867,  Lauder  Brunton  tried  the  effect  of  inhalations  of  this  substance  upon  patients 
suffering  from  an  acute  attack  of  angina  pectoris,  and  demonstrated  that  it  produced  very 
marked,  almost  instantaneous  relief.  He  was  led  to  investigate  this  substance  by  the 
realization  that  the  attack  was  accompanied  by  vasoconstriction  and  high  blood-pressure, 
and  bj'^  the  knowledge  that  the  newly  investigated  amyl  nitrite  had  been  found  to  have 
a  vasodilator  action.  Lauder  Brunton 's  observations  have  been  generally  confirmed,  and 
this  drug  has  become  the  classical  remedy  for  relief  of  the  attack.  Its  action  should  be 
supplemented  at  once  by  hypodermic  or  oral  administration  of  one  or  two  drops  of  spirits 
of  nitroglycerin  (or  more  if  the  patient  has  been  found  resistant  to  it),  and  this  may  be 
followed  by  erythrol  tetranitrate  by  the  mouth,  since  this  drug  exerts  a  slower  action 
lasting  over  three  to  six  hours.  Erythrol  tetranitrate  should  be  continued  for  some  time 
after  the  attack. 

Potassium  Iodide.  —  Between  attacks  potassium  iodide  in  moderate 
doses — 0.3  Gm.  (gr.  v)  to  4  Gm.  (3i)  t.i.d. — should  be  given,  as  it  seems  to 
diminish  the  frequency  and  severity  of  attacks. 

Dr.  G.  S.  Bond  in  the  writer's  laboratory  has  found  that  practically  all  the  drugs 
which  he  has  investigated  affected  the  outflow  from  the  coronary  veins  in  the  dog's  heart 
exactly  as  they  affected  the  general  blood-pressure.  Amyl  nitrite  and  nitroglycerin  were  no 
exceptions  to  this  rule.  They  lowered  the  general  blood-pressure  and  decreased  the  outflow 
through  the  coronaries.  The  effect  -was  the  same  whether  the  heart  was  dilated  or  not, 
and  seemed  also  to  be  independent  of  the  strength  of  the  heart.  In  view  of  these  findings, 
it  must  be  borne  in  mind  that  Hewlett  has  found  that  a  rise  in  blood-pressure  fol- 
lows quite  uniformly  within  one  minute  after  the  inhalation  of  amyl  nitrite  is  begun. 
Whether  it  is  the  fall  of  blood-pressure  or  the  rise  of  blood-pressure  which  is  accompanied 
by  increased  flow  through  the  coronary  vessels  after  the  inhalation  cannot  be  regarded  as 

'  Perhaps  this  may  bring  with  it  a  dilatation  of  the  coronary  arteries. 


296  DISEASES   OF   THE   HEART   AND    AORTA. 

certain.  It  must  be  admitted,  however,  that  in  Bond's  experiments  the  coronary  arteries 
were  not  in  a  state  of  vasomotor  spasm,  and  therefore  the  analogy  is  not  an  absolute  one. 
It  is  also  probable  that  the  mere  lowering  of  the  general  blood-pressure,  independently 
of  any  action  upon  the  coronaries,  tends  in  itself  to  relieve  the  cardiac  dilatation  by  dimin- 
ishing the  work  of  the  heart. 

Caffeine,  Theobromine,  and  Theophylline.  —  Caffeine  and  especially 
theobromine  and  theophylline  preparations — especially  acettheobromine 
sodium  ("agurin")  and  acettheophylline — have  been  highly  recommended, 
from  the  clinical  stand-point,  by  Askanasy,  Kaufmann  and  Pauli,  R.  Breuer, 
Buch,  Pineles,  v.  Leyden,  and  others,  to  relieve  and  to  ward  off  the  attacks 
of  stenocardia. 

Oswald  Loeb  has  given  an  experimental  basis  to  these  observations  by  demonstrat- 
ing on  the  excised  heart  that  these  drugs  increase  the  blood  flow  through  the  coronary 
vessels  as  well  as  increase  the  systolic  output  and  the  force  of  the  heart-beat.'  Theobromine 
and  theophylline  are  to  be  preferred  to  caffeine,  since  they  do  not  increase  peripheral 
resistance  and  have  little  action  upon  the  higher  nervous  centres,  but,  on  the  other  hand, 
a  more  marked  action  on  the  coronary  arteries.  On  the  other  hand,  they  are  not  very 
certain  in  producing  their  effect.  They  may  be  helpful  in  some  cases  and  may  absolutely 
fail  in  others,  and,  while  they  are  worthy  of  a  trial  in  almost  every  case,  they  cannot  as 
yet  be  expected  to  supplant  the  nitrites  and  iodides. 

Diet.  —  Diet  is  all-important.  It  should  be  chiefly  lactovege- 
t  a  r  i  a  n  in  character.  The  meals  should  be  small  in  amount,  to 
prevent  overloading  and  distention  of  the  stomach  and  hence  the  pushing 
up  of  the  diaphragm.  Gastric  fermentation  should  be  prevented 
by  removing  from  the  diet  any  articles,  such  as  soft  hot  breads,  heavy  and 
greasy  pastry,  etc.,  which  may  be  found  to  produce  flatulence,  and  by 
general  treatment  of  the  gastric  condition.  Air -swallowing  should 
be  carefully  looked  for  and  treated  (see  page  604).  Meat  and  soups 
should  be  reduced  to  small  quantities,  since  they  contain  considerable 
quantities  of  purin  bodies  which  have  a  vasoconstrictor  action  and  which 
also  act  injuriously  upon  the  kidneys.  The  vegetable  and  cereal  foods 
should  make  up  the  bulk  of  the  diet.  Salt  should  be  reduced  for  the  same 
reason.    Liquids  should  be  restricted  to  about  1500  c.c.  a  day. 

Milk  may  be  a  staple  article  in  the  diet,  unless,  as  in  many  persons, 
it  tends  to  flatulence.  This  is  sometimes  obviated  by  adding  a  very  little 
weak  tea  or  coffee,  but  very  often  it  must  be  dispensed  with  altogether. 

Tobacco  should  be  absolutely  excluded  in  both  organic  and  func- 
tional cases. 

Tea  and  coffee  in  small  amounts  (one  cup  a  day,  very  weak)  probably 
have  very  little  effect  upon  the  average  individual  who  has  been  accustomed 
to  them,  but  may  be  quite  important  factors  in  bringing  on  the  attacks 
in  persons  whose  sensitiveness  is  a  little  above  normal  and  in  whom  there 
is  a  tendency  to  angina.    It  is  best  for  them  to  be  given  up. 

Local  Treatment  of  the  Chest  Wall. — Vigorous  counter-irritation  to 
the  chest  wall,  by  blistering,  etc.,  is  also  of  value,  and  Hasselbach  and 
Jacobaeus  report  very  marked  improvements,  lasting  a  year  or  so,  from 

'  Dr.  G.  S.  Bond,  in  the  writer's  laboratory,  has  been  unable  to  produce  any  appre- 
ciable change  in  the  outflow  from  the  coronary  veins  of  the  dog's  heart  in  situ;  and  with 
the  amyl  nitrite  and  nitroglycerin  observed  a  marked  decrease  in  the  outflow,  even  when 
the  animal's  heart  was  dilated. 


ANGINA   PECTORIS.  297 

exposure  of  the  precordium  to  the  Finsen  Ught  for  an  hour  a  day  until  a 
marked  cutaneous  reaction  or  even  bUstering  has  set  in. 

Electrical  Treatment. — J.  0.  Hirschfelder  states  that  in  five  cases  he 
has  obtained  striking  relief  of  the  symptoms  by  treatment  with  the 
galvanic  current,  applying  the  anode  (a  pad  4  cm.  in  diameter) 
to  the  neck  over  the  course  of  the  vagus,  and  the  cathode  (6-12  cm. 
in  dianeter)  to  the  precordium,  and  passing  a  current  of  2  0  m  i  1 1  i  a  m  - 
p  e  r  e  s  for  five  minutes  to  each  side  of  the  neck.  One  patient  remained 
free  from  attacks  until  his  death  two  years  after  the  treatment;  another  has 
remained  free  for  several  years.  In  the  other  three  the  relief  was  less 
permanent,  but  still  very  gratifying. 

In  other  cases  the  use  of  electric  baths,  and  especially  with  the 
sinusoidal  current,  may  be  of  value  (Rumpf),  but  the  effect  is 
readily  overdone.  The  alternating  current  is  certainly  much  less  soothing 
than  the  sinusoidal. 

BIBLIOGRAPHY. 

Porter,  W.  T. :  On  the  Results  of  Ligation  of  the  Coronary  Arteries,  J.  Physiol.,  Canib., 

1893,  XV,  12L 
Magrath,  G.  B.,  and  Kennedy,  H.:  On  the  Relation  of  the  Volume  of  the  Coronary  Circula- 
tion to  the  Frequency  and  Force  of  the  Ventricular  Contraction  in  the  Isolated  Heart 

of  the  Cat,  J.  Exp.  Med.,  N.  Y.,  1897,  ii,  13. 
Cohnheim,  J.,  and  v.  Schulthess  Rechberg,  A.:  Ueber  die  Folgen  der  Kranzarterienver- 

schliessung  fiir  das  Herz.,  Arch.  f.  path.  Anat.,  etc.,  Berl.,  1881,  Ixxxv,  503. 
Panum:  Experimentelle  Beitrage  zur  Lehre  von  der  Enibolie,  ibid.,  1862,  xxv,  308  and  433. 
Baumgarten,  W. :  Infarction  in  the  Heart,  Am.  J.  Physiol.,  Bost.,  1899,  ii,  243. 
Hirsch,  C,  and  Spalteholz,  W. :  Coronarterien  und  Herzmuskel,  Deutsch.  med.  Wochen- 

schr.,  Berl.,  1907,  xxxiii,  790. 
Pratt,  F.  H. :  The  Nutrition  of  the  Heart  through  the  Vessels  of  Thebesius  and  the  Coronary 

Veins,  Am.  J.  Physiol.,  Bost.,  1898,  i,  86. 
Porter,  W.  T. :  The  Influence  of  the  Heart-beat  on  the  Flow  of  Blood  through  the  Walls  of 

the  Heart,  ibid.,  1898,  i,  145. 
Maass,   P.:  Experimentelle  Untersuchungen   iiber  die   Innervation   der  Kranzarterienge- 

fasse  des  Saugethierherzens,  Arch.  f.  d.  ges.  Physiol.,  Bonn,  1899,  Ixxiv,  281. 
Langendorff,  O. :  Ueber  die  Innervation  der  Koronargefasse,  Zentralbl.  f.  Physiol.,  Leipz. 

u.  Wien,  1907,  xxi,  551. 
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Walls  of  the  Heart,  Am.  J.  Physiol.,  Bost.,  1898,  i,  215. 
Halsted,  W.  S. :  The  Results  of  the  Complete  and  Incomplete  Occlusion  of  the  Abdominal 

and  Thoracic  Aortas  by  Metal  Bands,   J.   Am.  M.  Ass.,  Chicago,  1906,  xlvii,  2147. 

The   Partial  Occlusion  of  Blood-vessels,  Especially  of  the  Abdominal  Aorta,  Johns 

Hopkins  Hosp.  Bull.,  Baltimore,  1905,  xvi,  346. 
Also  Miller,  J.  L.,  and  Matthews,  S.  A.:  Effect  on  the  Heart  of  Experimental  Obstruction 

of  the  Left  Coronary  Artery,  Arch.  Int.  Med.,  Chicago,  1909,  iii,  476. 
Romberg,  E.:  Lehrbuch  der  Krankheiten  des  Herzens,  Stuttgart,  1906,  115. 
Lewis,  T. :  Paroxysmal  Tachycardia,  Heart,  Lond.,  1909,  i,  42. 
Jellinek,  E.  O.,  and  Cooper,  C.  M.:  Cardiac  Asthma  and  Sclerosis  of  the  Right  Coronary 

Artery,  J.  Am.  M.  Asso.,  Chicago,  1908,  1,  689. 

Angina  Pectoris. 

Heberden,  Wm.:  Commentaries  on  the  History  and  Cures  of  Disease,  Philadelphia,  1845. 
Home,  Everard:  Life  of  Hunter,  prefixed  to  the  "Treatise  on  Inflammation,"  1794,  p.  45. 

Quoted  from  Sir  W.  T.  Gairdner's  article  on  "Angina  Pectoris  and  Allied  States" 

in  Reynolds's  System  of  Medicine,  Philadelphia,  1877,  iv,  534. 
Baron:  Life  of  Jenner,  London,  1827.    Quoted  from  W,  Osier's  "Angina  Pectoris  and  Allied 

States,"  N.  York,  1897. 


298  DISEASES   OF   THE   HEART   AND    AORTA. 

Gairdner,  W.  T.:  Angina  Pectoris  and  Allied  States,  in  "A  System  of  Medicine,"  edited 

by  J.  Russell  Reynolds,  Phila.,  1877,  iv,  534. 
Osier,  W.:  Lectures  on  Angina  Pectoris  and  Allied  States,  N.  York,  1897. 
Gibson,  G.  A.:  The  Nervous  Affections  of  the  Heart,  Edinb.  and  Lond.,  1905. 
Ludwig  and  Cyon:  Ber.  d.  k.  Sachs  Gesellsch.  d.  Wissensch.  math.  phys.  CI.,  Leipz.,  1886, 

307.     Quoted  from  Shafer's  Physiology. 
Eyster,  J.  A.  E.,  and  Hooker,  D.  R.:  Vagushemmung  bei  des  Blutdruckes,  Zentralbl.  f. 

Physiol.,  Leipz.,  1908,  xxi. 
Mackenzie,  James:  Heart  Pain  and  Sensory  Disorders  associated  with  Heart  Failure, 

Lancet,  Lond.,  1895,  i,  16. 
Head,  H.:  Pain  in  Visceral  Disease,  Brain,  Lond.,  1893,  xvi,  1;    1894,  xvii,  339;    1896, 

xix,  153. 
Head,  H.,  Rives,  W.,  and  Sherren,  Jr.:  The  Afferent  Nervous  System  from  a  New  Aspect, 

ibid.,  1905,  xxviii,  99.     Sherren,  J.:  Some  Surgical  Observations  on  Referred  and 

Reflected  Pain,  Clin.  J.,  Lond.,  1905,  xxxvi,  168.    Abstracted  in  editorial,  J.  Am.  M. 

Ass.,  Chicago,  1909,  lii. 
Head,  H.,  and  Thompson,  Th.:  The  Grouping  of  Afferent  Impulses  within  the  Spinal  Cord, 

ibid.,  1906,  xxix,  536. 
Harvey,  Wm.:  The  Works  of  Wm.  Harvey,  trans,  by  R.  Willis.    Printed  for  the  Sydenham 

Soc.,  Lond.,  1847,  382. 
Hirschfelder,  A.  D.:  Observations  on  a  Case  of  Palpitation  of  the  Heart,  Bull.  Johns 

Hopkins  Hosp.,  Baltimore,  1906,  xvii,  299. 
Huchard,  H.:  Traite  clinique  des  maladies  du  cceur  et  de  I'aorte,  3d  edit.,  Paris,  1899, 

ii,  p.  1  et  seq. 
Ratner,  Lee.     Quoted  on  p.  613. 
Jackson, D.  E.,  and  Matthews,  S.  A.:  The  Sensory  Nerves  of  the  Heart  and  Blood-vessels 

as  a  Factor  in  Determining  the  Action  of  Drugs,  Am.  J.  Physiol.,  Bost.,  1908,  xxv,  255. 
Lancereaux:  De  I'alteration  de  I'aorte  et  du  plexus  cardiaque  dans  I'angine  de  poitrine, 

Compt.  rend.  Soc.  de  biol..  Par.,  1864,  4  s.,  i,  15. 
Grocco,  P.:  Sull  angina  di  petto,  Settimana  Med.  di  Sperimentale,  Firenze,  1896,  i,  1,  13, 

109,  169,  181. 
Benenati,  U.:  Sull'  origine  nevritica  dell'  angina  pectoris  da  aortite  sifilitica,  Riforma 

Med.,  Roma,  1902,  xviii,  326,  339,  351. 
Mott,  F.  W.     Quoted  from  Oliver,  Th.:     A  Lecture  on  Angina  Pectoris  and  Allied  Con- 
ditions, Lancet,  Lond.,  1905,  ii,  812. 
Herard:  Angine  de  poitrine  caracterisee  anatomiquement  par  un  retrecissement  considera- 
ble des  deux  arteres  coronaires  a  leur  origine  sans  lesions  des  plexus  cardiaques,  Bull. 

Acad,  de  Med.,  Par.,  1883,  2  ser.,  xii,  1522. 
Latham,  J.:  Med.  Trans.  Roy.  Coll.  Phys.,  Lond.,  1812.    Quoted  from  Gibson. 
Nothnagel,  H.:  Angina  pectoris  vasomotoria,  Deutsch.  Arch.  f.  kUn.  Med.,  Leipz.,  1867, 

iii,  309. 
Osier,  W. :  Angina  Pectoris  as  an  Early  Sign  in  Aneurism  of  the  Aorta,  Med.  Chron.,  Man- 
chester, 1906,  Ixiv,  69. 
Lauder-Brunton,  T.:  On  the  Use  of  Nitrite  of  Amyl  in  Angina  Pectoris,  Lancet,  Lond., 

1867,  ii,  97. 
Askanazy:  Klinisches  ueber  Diuretin,  Deutsch.  Arch.  f.  klin.  Med.,  Leipz.,  Ivi,  209. 
Kaufmann  and  Pauli:    Zur  Symptomatologie  des  stenokardischen  Anfalles,  Wien.  klin. 

Wchnschr.,  1902,  xv,  1160. 
Breuer,  R.:  Zur  Therapie  und  Pathogenese  der  Stenokardie  und  verwandter  Zustande, 

Miinchen.  med.  Wchnschr.,  1902. 
Pineles,  Fr.:  Theocinbehandlung  stenokardischer  Anfalle,  Mitth.  d.  Gesellsch.  f.  inn.  Med., 

Wien,  1903-1904.     (Quoted  from  Pal.) 
Leyden,  E.  v.:  Fiinfzig  Jahre  innerer  Therapie,  Therap.  d.  Gegenw.,  Berl.,  1909,  1,  1. 
Hasselbach,  H.  A.,  and  Jacobaeus,  H.:  Ueber  die  Behandlimg  von  Angina  Pectoris  mittelst 

starken  Kohlbogenlichtbadern,  Berl.  klin.  Wchnschr.,  Berl.,  1907,  xliv,  1247. 
Hirschfelder,  J.  O.:  Personal  communication. 
Rumpf:  Zur  Einwirkung  oszillierender  Strome  auf  das  Herz,  Zentralbl.  f.  innere  Med., 

Leipz.,  1907,  xxviii,  441. 


PART   III. 


ENDOCARDITIS. 

In  spite  of  the  greater  frequency  of  arteriosclerosis  and  myocarditis, 
■the  clinical  pictures  of  valvular  diseases  are  so  much  more  definite  as  to 
render  them  the  most  striking  of  all  diseases  of  the  heart.  They  constitute 
indeed  a  large  percentage  of  all  diseases  seen  by  the  physician,  numbering 
1781  (7.6  per  cent.)  of  the  23,200  cases  admitted  to  the  medical  service 
of  the  Johns  Hopkins  Hospital  from  1889  to  1908. 


HISTORICAL. 

Vieussens  in  1715  described  lesions  of  the  valves  occurring  in  the  form  of  warty  or 
cauhfliower  excrescences  or  vegetations,  which  prevented  the  closure  of  the  valves.  Vir- 
<!how  called  attention  to  the  fact  that  as  a  rule  these  vegetations  were  not  situated  at  the 
margins  of  the  cusps,  but  at  a  little  distance  from  the  margin,  at  the  line  of  closure  where 
the  cusps  struck  together,  at  the  point  where  injury  to  the  endothelial  cells  was  most  likely 
to  occur.  That  this  injury  was  usually  due  to  the  action  of  bactei  ia  was  shown  when  Winge 
and  Heiberg  and  Virchow  in  1869  demonstrated  microscopically  the  presence  of  minute 
granules  within  the  vegetations.  In  1883  Weichselbaum 
cultivated  staphylococci  and  streptococci  from  endocardial 
vegetations,  and  his  pupil  Wyssokowitch,  as  well  as  Orth 
and  Ribbert,  produced  them  experimentally  in  animals  by 
the  injection  of  bacteria  into  the  blood. 

PATHOLOGICAL    ANATOMY. 

Development  of  the  Lesions. — Mechanical  or 
toxic  injury  is  an  important  factor  in  bringing 
about  these  lesions  upon  the  valves.  Indeed 
Wyssokowitch  found  that  his  experiments  suc- 
ceeded only  after  he  had  punctured  or  injured 
the  valves  with  probes;  while  Ribbert  supplied 
the  mechanical  factor  by  injecting  emulsions 
•of  potato  cultures  which  contained  small  masses 
of  potato  that  hurled  themselves  against  the 
valves.  Prudden,  on  the  other  hand,  found 
that  infection  of  the  valves  took  place  in  much 

the  same  way  if  the  valves  had  been  injured  with  chemical  substances. 
The  fibrinous  exudate  is  exudated  rapidly  after  the  injury,  and  is  whipped 
into  strands  by  the  action  of  the  current,  so  that  within  one  hour  after 
mechanical  injury  of  the  aortic  valve  a  mass  of  fibrin  having  the  cauliflower 
shape  of  a  vegetation  may  be  found  filling  the  hole  in  the  valve  (Hirschfelder) . 

299 


Fig.  170.  —  Fibrinous  deposit 
upon  an  aortic  cusp  one  hour  after 
mechanically  injuring  the  valve, 
showing  liow  the  cauliflower- 
shaped  mass  of  fibrin  tends  to  plug 
the  hole  in  the  valve.  (Kindness 
of  the  Johns  Hopkins  Hospital 
Bulletin.) 


300 


DISEASES   OF   THE   HEART   AND    AORTA. 


Ulcerative  Endocarditis. — The  fate  of  this  fibrinous  exudate  and  the 
type  of  the  lesion  varies  with  the  virulence  of  the  germ.  If  the  virulence 
is  high  the  lesion  is  often  large  and  may  involve  the  walls  of  the  auricle 
or  ventricle  (mural  endocarditis)  as  well  as  the  cusps  of  the  valve  (valvu- 
litis) .  The  necrosis  spreads  into  the  deeper  tissues  of  the  valve  or  even 
penetrates  through  it,  and  the  vegetation  consists  of  a  mass  of  degenerated 
fibrin,  clumps  of  bacteria,  and  necrotic  tissue  (Fig.  174)  rich  in  polymor- 
phonuclear leucocytes.  Under  the  influence  of  the  ferments  which  these 
secrete,  the  masses  become  partly  liquefied,  so  that  their  attachment  to 
the  cusps  is  loosened  and  they  may  be  readily  swept  off  as  emboli  by  the 
force  of  the  blood  stream  only  to  cause  infarction  and  abscesses  in  dis- 
tant tissues.  Such  emboli  naturally 
vary  in  size  from  a  small  bit  of  fibrin 

barely  capable  of  plugging  a  capillary               ,       \          j           ^  I 

to   a   mass   almost  the   size   of  the  ,      '\.''  )        lilg-.a«^ ^'L  Ma 


Fig.  171.  —  Mitral  endocarditis  showing  large 
vegetations.  A,  mural  portion  of  the  vegetations; 
B,  vegetations  along  line  of  closure. 


Fig.  172. 


-Injection  of  chronically  inflamed  valves. 
(After  V.  Langer.) 


valve  itself.  However,  they  rarely  reach  the  tremendous  size  attained  by 
the  non-septic  emboli  which  arise  from  intra-vitam  thrombi  in  the  auricles. 
Chronic  Endocarditis. — When  the  bacteria  upon  the  valves  are  less 
virulent  or  the  immunity  of  the  patient  develops,  a  different  process  occurs. 
The  areas  of  necrosis  are  smaller  and  are  walled  off  with  leucocytes.  Later 
these  give  place  to  the  fibroblasts  and  plasma  cells  of  chronic  inflammation, 
which  in  turn  are  replaced  by  strands  of  newly  formed  connective  tissue, 
which  push  out  into  the  exudate  and  finally  replace  it  altogether,  leaving 
a  solid  vegetation  composed  entirely  of  fibrous  tissue.  With  the  ingrowth 
of  connective  tissue  blood-vessels  penetrate  into  the  vegetation,  entering 
it  from  the  subendocardial  layers  of  myocardium  just  as  they  enter  scle- 
rotic patches  in  arteriosclerosis  (Koester,  v.  Langer,  Darier,  Ribbert),  Fig. 
172.  As  healing  becomes  complete  the  endothelial  layer  of  the  intima 
slowly  grows  in  from  the  periphery  and  gradually  covers  the  entire  vegeta- 


ENDOCARDITIS. 


301 


tion.  This  relining  of  the  vegetation  with  endothehum  is,  from  a  prog- 
nostic stand-point,  a  most  important  step  in  the  heahng,  for,  as  Wyssoko- 
witch  has  shown,  infection  occurs  most  readily  when  the  surface  of  the 
valve  is  injured,  and  clinical  experience  shows  that  a  valve  once  injured 
is  particularly  liable  to  rein- 
fection. Thus,  it  is  common  to 
find  a  fresh  ulcerative  endo- 
carditis occurring  upon  a  valve 
which  is  already  the  subject  of 
a  chronic  endocarditis,  several 
different  stages  appearing  upon 
the  same  specimen. 


Muscular  tissue 


Fibro- 
elastic 
tissue  of 
valve- 
leaflef 


Chordae 
tendiiieae 


INFECTIVE    AGENTS. 

The  most  important  infec- 
tive agents  in  the  causation  of 
endocarditis  are  the  micro- 
coccus of  rheumatic  fever, 
the  pyogenic  cocci,  the 
pneumococcus,  the  gono- 
coccus,  the  bacillus  influ- 
enzae, and  the  spirochaete 
pallida  (triponema  pallidum) 
of  syphilis. 

Rheumatism. — By  far  the 
most  frequent  cause  of  heart 
disease  is  rheumatism,  which 
gave  rise  to  62.6  per  cent,  of 
Border's  cases  of  malignant 
endocarditis,  and  occurs  in 
about  the  same  percentage  in 
the  milder  forms.  However, 
the  exact  causal  factor  of  rheu- 
matism itself  is  not  yet  settled. 
Sahli  in  1893  isolated  what  he 
thought  to  be  a  staphylococcus 
from  joints,  endocardium,  and 
the  heart's  blood  of  patients 

dying  of  acute  non-suppurative  arthritis,  and  then  stated  that  he 
garded    acute    articular  rheumatism   as    an    infectious 
ease  due  to  the   action  of   attenuated   pyogenic   cocci. 

Recently  Menzer  and  Rufus  Cole  have  revived  this  view,  and  the  latter  has  produced 
non-suppurative  arthritis  and  endocarditis  in  rabbits  by  the  injection  of  streptococci  from 
various  sources,  showing  also  that  in  the  joints  these  assume  the  diplococcus  arrangement. 

Triboulet,  Wassermann,  Westphal  and  Malkoff,  and  Poynton  and  Paine,  however, 
regard  the  micrococcus  (diplococcus)  which  they  have  obtained  in  cases  of  the  rheumatic 

1  "  .  .  .  Auffassung  des  Gelenk  rheumatismus  als  einer  auf  der  Wirkung  abge- 
schwachter  pyogenen  Kokkenberuhenden  Infektionskrankheit." 


Fig. 


173. — Structure   of    the    normal    aui  iculoventricular 
valve.      (After  Piersol.) 


(  c 


re- 
dis- 

!  1  1 


302 


DISEASES   OF   THE   HEART   AND    AORTA. 


cycle  as  a  specific  organism  or  at  least  a  specific  strain,  thotigh  Walker  has  show,-n  that  its 
cultural  characteristics  are  by  no  means  sharply  defined.  The  micrococcus  (rheumaticus) 
of  Poynton  and  Paine  assumes  the  diplococcus  form  in  the  joints  but  becomes  a  strep- 
tococcus in  culture  media,  just  as  Cole  found  for  many  ordinary  streptococci.  Beattie  and 
Longcope  also  have  isolated  what  they  believe  to  be  the  micrococcus  of  Poynton  and  Paine 
from  cases  of  arthritis  with  endocarditis  and  have  produced  both  conditions  in  animals. 
Poynton  has  obtained  the  same  germ  from  the  cerebral  cortex  in  simple  chorea  and  from 
the  tonsils.  Meakins,  on  the  other  hand,  has  found  large  foci  of  streptococci  in  the  tonsils 
which  have  been  removed  from  patients  having  rheumatism,  but  these  germs  do  not  show 


Fig.  174. — Photomicrograph  of  a  specimen  showing  acute  and  subacute  endocarditic  lesions  upon 
the  mitral  valve.  A.  Entire  specimen  (low  power).  B.  Outline  sketch  showing  the  portions  from  which 
C,  D,  and  E  are  taken.  C.  Margin  of  the  area  of  acute  endocarditis  (high  power).  D.  Ulcerating  area, 
showing  masses  of  necrotic  tissue  and  exudate.  E.  Area  where  the  process  is  more  chronic,  showing 
strands  of  newly-formed  fibrous  tissue  entering  the  vegetation. 


any  uniformity  which  would  permit  them  to  be  identified  with  the  strain  of  Poynton  and 
Paine.  These  points  tend  to  favor  the  original  view  of  Sahli  that  rheumatism  is  not  due 
to  a  single  strain  but  to  a  variety  of  attenuated  cocci,  and  is  therefore  to  be  regarded  as 
a  clinical  group  of  diseases  rather  than  as  a  single  disease. 

The  Pyogenic  Cocci. — The  pyogenic  cocci  of  puerperal  fever,  abscess, 
and  septicaemia  are  also  very  common  causes  of  endocarditis.  They  are 
identified  with  special  frequency  in  the  malignant  forms,  owing  to  the  readi- 
ness with  which  they  are  then  cultivated,  but  there  seems  little  doubt  that 
less  virulent  strains  are  responsible  for  cases  of  chronic  endocarditis  as  well. 


ENDOCARDITIS. 


303 


Pneumococcus.  —  Wells  found  that  the  pneumococcus  caused  endo- 
carditis in  4  per  cent,  of  his  517  autopsies  upon  cases  dying  of  pneumonia, 
and  hence  the  latter  disease  is  a  relatively  frequent  cause  of  endocarditis. 
Lenhartz  states  that  the  endocarditis  often  arises  as  a  recrudescence  after 
the  fever  from  the  original  pneumonia  has  subsided  (13th  to  15th  day), 
and  that  it  is  often  malignant  and  accompanied  by  meningitis. 

Gonococcus. — The  importance  of  the  gonococcus  in  producing  endo- 
carditis as  well  as  rheumatism  is  growing  from  year  to  year. 


CHOREA 


TONSILLITIS 


ARTHRITIS 


FiQ.  175. — Portals  of  infection  in  endocarditis.   (Schematic.) * 


The  clinical  association  of  endocarditis  and  urethritis  was  recognized  by  Ricord  in 
1847  and  by  Brandes  in  1854.  V.  Leyden  in  1893  demonstrated  upon  the  valves  cocci 
which  decolorized  by  Gram's  method,  but  the  first  positive  cultures  of  the  gono- 
coccus from  the  blood  during  life  were  made  at  the  Johns  Hopkins  Hospital  by  Thayer 
and  Blumer  in  1895.  Since  then  the  condition  has  been  found  frequently,  and  should 
always  be  sought  for  in  cases  of  gonorrhcBal  rheumatism. 

Miscellaneous  Infections. — Occasionally  endocarditis  arises  during  or 
after  diphtheria,  scarlet  fever,  and  smallpox,  though  in  these  cases,  as  in 
tuberculosis,  the  lesion  is  probably  most  frequently  produced  by  strepto- 
cocci which  are  present  as  a  mixed  infection.  True  tuberculous  endocarditis 
is  rare  (Marshall),  though  it  has  been  produced  experimentally  in  animals 
(Michaelis  and  Blum). 

The  bacillus  of  influenza  is  also  an  important  factor  (Austin),  though 
less  frequent  in  endocarditis  than  in  myocarditis. 

'  The  term  micrococcus  rheumaticus  is  used  for  convenience,  but  with  all  reservations 
as  to  possible  specificity. 


304  DISEASES   OF  THE   HEART   AND   AORTA. 

Syphilis. — Whether  true  valvular  lesions  are  produced  by  the  spiro- 
chaete  pallida  of  syphilis  has  not  been  absolutely  proved,  but  recently 
Collins  and  Sachs  and  Longcope  have  obtained  a  positive  Wassermann 
reaction  in  a  large  percentage  of  cases  of  aortic  insufficiency  in  which  the 
valves  were  puckered,  shrunken,  and  calcified.  In  these  cases  it  is  not  the 
intima  but  the  middle  fibro-elastic  layer  of  the  valves  in  which  the  change 
goes  on,  exactly  analogous  and  usually  coincident  with  similar  changes  in 
the  deejjer  layers  of  the  intima  and  media  of  the  aorta. 

Sclerotic  and  Atheromatous  Lesions  of  the  Endocardium.  —  Besides 
these  forms  of  endocarditis  there  seems  to  be  a  certain  number  of  cases, 
especially  of  lesions  about  the  aorta,  in  which  sclerosis  and  calcification 
take  place  in  the  fibro-elastic  layer  of  the  valves  exactly  as  in  the  luetic 
lesion,  but  in  which  the  patient  has  never  had  a  luetic  infection  (as  in  the 
case  of  J.  L.,  page  467).  The  similarity  here  is  exactly  like  that  between 
luetic  and  non-luetic  arteritis,  as  shown  by  Ophiils,  and  needs  no  further 
comment. 

PATHOLOGICAL    PHYSIOLOGY. 

The  disturbances  in  heart  action  due  to  endocarditis  may  depend 
upon  three  immediate  causes; 

(1)  The  mechanical  effects  due  to  leaks  or  obstructions  at  any  of  the  valvular  orifices. 
(This  will  be  discussed  in  detail  in  connection  with  each  of  the  chronic  valvular  lesions.) 

(2)  The  weakening  of  the  heart  muscle  due  to  the  acute  myocarditis  and  the  fatty 
and  parenchymatous  changes  in  the  muscle  cells,  resulting  from  the  direct  invasion  of  the 
muscle  by  the  cocci,  from  effect  of  their  toxins  upon  it,  and  from  the  ansemia  which  fre- 
quently accompanies  the  infection. 

(3)  The  weakening  of  the  heart  which,  as  in  other  febrile  and  infectious  diseases, 
results  from  lowering  of  vasomotor  tone,  and  which  is  brought  about  by  a  relative  empti- 
ness of  the  blood-vessels.    This  is  accompanied  by  low  blood-pressure  and  rapid  pulse. 

.  In  the  chronic  forms  of  carditis  the  first  is  the  most  important  factor; 
while  in  the  simple  acute  and  the  malignant  forms  the  two  latter  frequently 
outweigh  it,  so  that  there  may  be  few  symptoms  referable  to  the  local 
mechanical  effects  upon  the  circulation. 

Effects  on  the  Circulation. — The  physical  signs  will  be  discussed  par- 
ticularly in  the  case  of  individual  valvular  lesions;  but  in  general  it  may 
be  said  that  a  leak  at  an  orifice  necessitates  an  increase  in 
the  output  of  the  chamber  in  order  to  compensate  for  the 
amount  regurgitating  or  an  increase  in  force  of  contraction  of  the  cham- 
ber behind  it.    Thus,  in  mitral  insufficiency, 

Ventricular    systolic    output  =  Output    into    aorta  +  Backflow 
into  auricle; 

while  in  aortic  insufficiency 

Ventricular    systolic     output  =  Output    into    aorta  =  Outflow 
through  peripheral  vessels  +  Backflow  into  ventricle. 

In  either  of  these  cases  the  circulation  may  be  maintained  either  by  increasing  this  output 
per  beat  or  by  increasing  the  heart-rate;  and  in  neither  of  these  cases  is  the  pulse-pressure 
proportional  to  the  systoUc  output  of  the  ventricle. 

On  the  other  hand,  when  a  valvular  orifice  is  narrowed  it  may  have  little  or  no  effect 
until  the  narrowing  reaches  a  certain  point;  for,  though  it  slows  the  inflow  or  the  outflow, 
as  the  case  may  be,  yet  the  duration  of  systole  or  of  diastole  may  be  sufficiently  great  to 


ENDOCARDITIS. 


305 


permit  of  complete  filling  or  emptying  during  the  time  available;  but  beyond  this  greater 
driving  power  is  needed  and  the  chamber  behind  the  stenosis  must  undergo  hypertrophy. 
Regurgitations  usually  cause  dilatation  of  the  chambers  into  which  the 
leak  occurs,  unless  a  great  increase  in  tonicity  of  the  muscle  has  caused  the  cavity 
actually  to  decrease  in  size  (Stewart,  Cameron,  Hirschfelder,  Cloetta). 

CLINICAL    GROUPING. 

Clinically,  endocarditis  (or  carditis^)  has  been  divided  by  Osier  into 
three  groups: 

(1)  The  malignant  type,  in  which  septic  and  highly  febrile  symp- 
toms, with  symptoms  also  due  to  septic  embolism  in  various  parts  of  the 
body,  dominate  the  clinical  picture,  and  in  which  the  cardiac  lesions  may 
spread  rapidly  and  involve  almost  all  the  valves.  This  is  usually  fatal 
during  the  acute  attack. 


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(2)  The  simple  acute  type,  in  which  one  or  two  valves  (the 
mitral  and  aortic)  are  affected,  but  where  the  lesions  remain  confined  to 
them.  The  salient  features  of  the  disease  are  not  those  due  to  high  fever 
and  embolism,  although  these  may  at  times  be  present,  but  those  usually 
produced  by  the  infective  agent;  and  in  addition  there  are  weakness,  an- 
orexia, and  anaemia,  some  respiratory  distress,  and  syncope  on  exertion. 

^  Carditis  =  inflammation    affecting    endocardium,   myocardium,    and   pericardium 
simultaneously. 
20 


306  DISEASES   OF  THE   HEART   AND    AORTA. 

Occasionally"  there  are  oedema,  enlargement  of  the  liver,  ascites,  precordial 
pain,  and  palpitation,  but  these  are  often  absent. 

(3)  Chronic  endocarditis  usually  follows  after  an  attack  of 
simple  acute  endocarditis,  although  it  may  set  in  insidiously  as  a  result  of 
progressive  sclerotic  changes  in  the  valves,  especially  in  association  with 
arteriosclerosis,  syphilis,  and  chronic  anaemias.  The  original  characteristics 
of  an  infectious  disease  have  subsided,  and  the  picture  is  entirely  due 
to  the  mechanical  effects  of  leaking  valves  and  weakened  heart  muscle; 
in  short,  to  slowing  of  the  circulation,  dyspnoea,  cough,  oedema,  digestive 
disturbances,  palpitation,  precordial  and  referred  pains. 

MALIGNANT    ENDOCARDITIS. 

PATHOGENESIS. 

Most  commonly  an  attack  of  malignant  carditis  is  not  the  first  heart 
disease  from  which  the  patient  has  suffered,  but  it  is  found  that  the  acute 
process  involves  a  valve  which  already  shows  marks  of  a  chronic  endocardi- 
tis. This  is  not  at  all  surprising,  since  Rosenbach,  Wyssokowitsch,  Hasen- 
feld,  and  others  have  shown  that  valves  once  injured  become  the  seat  of 
inflammatory  processes  much  more  readily  than  when  intact.  If  the 
original  lesion  is  a  very  chronic  one  and  the  vegetation  well  supplied  with 
blood-vessels  (Ribbert),  organization  of  the  exudate  may  go  on  even  more 
readily  than  in  an  intact  valve;  but  if  the  older  exudate  is  still  fibrinous 
or  fresh,  the  tendency  to  soften  and  ulcerate  is  greater  than  if  it  were  rest- 
ing upon  a  base  of  relatively  healthy  tissue. 

Often  the  second  and  malignant  infection  may  be  due  to  an  organism 
quite  different  from  that  producing  the  first,  so  that  one  frequently  finds 
a  malignant  endocarditis,  due  to  the  streptococcus,  the  pneumococcus,  or 
the  gonococcus,  attacking  vegetations  originally  of  rheumatic  origin. 

In  the  chronic  forms  of  valvular  lesion  the  symptoms  of  an  acute 
febrile  disease  have  disappeared,  and  are  replaced  by  clinical  pictures  with 
characteristic  forms  of  hypertrophy,  stasis,  and  murmurs. 

Occurrence  and  Distribution. — The  relative  rarity  of  malignant  endocarditis  is  shown 
by  the  fact  that  only  45  cases  have  occurred  among  23,200  admitted  to  the  Johns  Hopkins 
Hospital  (0.19  per  cent.),  as  compared  with  1781  (7.6  per  cent.)  of  chronic  valvular  disease; 
also  by  the  statistics  of  Horder,  who  encountered  150  cases  among  19,904  patients  admitted 
to  St.  Bartholomew's  Hospital  (0.75  per  cent.).  The  occurrence  of  Horder's  150  cases  as 
regards  age  was  as  follows:  Under  5,  2  cases;  5  to  10  years,  5;  10-15  years,  9;  15-20 
years,  29;  20-30  years,  39;  30-40  years,  31;  40-50  years,  23;   50-60  years,  8;  over  60,  4. 

The  involvement  of  the  valves  was:  Mitral,  38;  aortic,  22;  mitral  and  aortic,  63; 
tricuspid  and  mitral,  14;  pulmonary  and  mitral,  7.  There  were  mural  auricular  lesions 
in  43;  mural  ventricular  in  8;   congenital  heart  lesions  in  8. 

Other  signs  and  complications  were:  Enlarged  spleen,  47;  heart  failure,  66;  haema- 
turia  (sometimes  only  microscopic),  46;  petechias,  43  (on  legs  only  in  10);  brain  symp- 
toms in  22  (choreiform  movements  in  7 ;  retinal  hemorrhages  noted  in  5,  though  certainly 
more  frequent);   embolic  aneurisms.  20. 

TYPES    OF    MALIGNANT    ENDOCARDITIS. 

Osier  in  his  masterly  lectures  has  divided  the  cases  of  malignant 
endocarditis  into  three  chnical  groups,  which  may  present  both  acute 
and  chronic  forms. 


ENDOCARDITIS.  307 

1.  The   septicaemic,   in  which  the  symptoms  are  primarily  those  of  septicaemia. 

2.  The  t  y  p  h  o  i  d  a  1  type,  which  closely  resembles  severe  typhoid  fever  or  acute 
miliary  tuberculosis, — continuous  high  fever,  enlarged  spleen,  and  absence  of  other  local- 
ized symptoms. 

3.  The  cerebral  type,  dominated  by  embolism  of  the  brain,  coma,  meningitis, 
paralyses. 

Septicaemic  Type. — The  septicsemic  type  is  the  most  common  and 
typical,  usually  following  abscess,  puerperal  fever,  operation,  wounds, 
occasionally  tonsillitis  or  quinsy,  or  some  other  definite  infection,  and  is 
characterized  by  prostration,  anorexia,  malaise,  frequently  headaches,  and 
shaking  chills.  In  Horder's  150  cases  the  fever  was  continued  in 
12,  irregular  and  intermittent  in  37,  quotidian  in  40,  absent  in  5.  The 
temperature  sometimes  fell  for  a  period  before  death.  The  complexion 
has  the  sallow  yellowish  color  of  haematogenous  jaundice,  there  is  rapidly 
progressing  increasing  anaemia,  and  the  eyes  are  dull.  There  is  sometimes 
acute  purulent  conjunctivitis,  sometimes  disturbances  of  vision  or  even 
blindness  due  to  the  presence  of  minute  emboli  or  hemorrhages  upon  the 
retina.  The  cheeks  are  sunken;  the  skin  is  usually  dry  except  during  the 
rigor  (in  contrast  to  the  drenching  sweats  of  rheumatic  fever) ;  the  tongue 
is  dry  and  furred;  the  lungs  may  be  clear  or  septic  bronchopneumonia  may 
be  present.  Respiration  is  usually  rapid.  The  signs  over  the  heart  are 
variable.  In  some  cases  there  are  no  abnormalities  in  heart  sounds,  cardiac 
area,  or  in  pulsations,  except  for  a  rapid  pulse-rate,  and  then  the  diagnosis 
may  long  remain  obscure;  or,  on  the  other  hand,  the  loudest  murmurs  may 
be  present  both  in  systole  and  in  diastole,  and  these  have  a  distribution 
corresponding  to  almost  any  of  the  valvular  lesions,  or  more  usually  to 
several  lesions  combined.  These  signs  often  change  markedly 
from  day  to  day,  corresponding  to  the  progression  of  the  lesion 
from  valve  to  valve,  the  growth  of  the  individual  vegetations,  or  the  dis- 
appearance of  the  latter  as  they  slough  off  into  the  blood  stream.  The 
pulse  is  small  and  collapsing,  but  usually  too  rapid  for  dicrotism,  and  the 
blood-pressure  is  low  (maximal  85  to  110  mm.,  minimal  60  to  90).  It 
becomes  larger  and  more  typically  water-hammer  in  character,  and  the 
diastolic  pressure  falls  to  40-50  mm.  if  a  leak  sets  in  at  the  aortic  valve. 
The  loud  systolic  murmur  over  the  tricuspid  area,  corresponding  to  tricuspid 
insufficiency  either  functional  or  organic,  is  among  the  most  common  in 
malignant  endocarditis,  for  this  valve  bears  the  brunt  of  both  the  increasing 
organic  lesions  and  the  progressive  weakening  of  the  heart  muscle.  Accom- 
panying this  there  is  also  systolic  pulsation  in  the  jugular  vein.  A  diastolic 
murmur  may  be  present  to  either  left  or  right  of  the  sternum,  and  may 
correspond  to  either  aortic  or  pulmonic  insufficiency,  the  distribution  in 
the  latter  case  being  somewhat  different  from  the  former.  A  pericardial 
friction,  associated  with  the  onset  of  fibrinous  or  purulent  pericarditis,  is 
not  uncommon. 

The  liver  is  frequently  enlarged,  either  from  cardiac  weakness  or 
from  a  definite  suppurative  hepatitis  and  cholangitis.  When  associated 
with  triscupid  insufficiency  it  may  pulsate  with  systole. 

The  spleen  is  often  enlarged,  from  the  presence  of  infarctions  of 
greater  or  less  extent.  The  abdomen  may  be  otherwise  normal  or  may 
be   tense,   and   there   may  be  local   tenderness  and   muscle   spasm  from 


308  DISEASES   OF   THE   HEART   AND    AORTA. 

localized  infection  or  general  peritonitis;  not  infrequently  these  areas 
correspond  to  the  uterus  (especially  in  puerperal  endocarditis)  or  to 
the  kidney,  owing  to  infarction,  in  which  case  there  are  also  albuminuria 
and  hsematuria. 

There  is  sometimes  oedema  of  the  extremities.  Arthritis  is 
frequent,  often  accompanied  by  injury  to  the  epiphyses  as  well  as 
the  joints,  and  occasionally  by  spontaneous  fractures.  The  skin  may  show 
very  numerous  small  purple  petechiae  or  large  areas  of  ecchymosis; 
or,  on  the  other  hand,  there  may  be  numerous  subcutaneous  abscesses  of 
varying  size. 

The  blood  count  is  usually  low,  especially  the  haemoglobin,  cor- 
responding to  the  type  of  a  secondary  ansemia.  Sometimes  500,000  ery- 
throcytes are  destroyed  each  day.  There  is  almost  always  a  polymorpho- 
nuclear leucocytosis  (20,000-30,000).  As  has  been  seen  blood  cultures  are 
positive  in  about  90  per  cent,  of  the  cases, — colonies  of  the  infective  agent, 
usually  20-40  per  cubic  centimetre  of  blood. 

The  urine  is  of  variable  amount,  and  specific  gravity  usually 
high.  It  generally  contains  albumen  and  casts,  and  often  there  is  definite 
hsematuria  due  to  infarction  of  the  kidney.  Sometimes  the  blood  can  be 
seen  only  with  the  microscope.  Not  infrequently  there  is  cystitis  with 
cocci  in  the  urine  in  considerable  quantities. 

Typhoidal  T}'pe. — The  cases  of  the  typhoidal  type  are  characterized 
also  by  asthenia,  by  high  fever  (103°  to  106°),  which  is  more  or  less  continu- 
ous, frequently  flushed  face,  dry  tongue,  sometimes  coma  vigil  and  picking 
at  bedclothes,  enlarged  spleen,  but  otherwise  no  definite  localizing  symp- 
toms. There  may  be  a  slight  bronchitis  or  small  foci  of  bronchopneumonia. 
The  cardiac  signs  may  be  indefinite,  or  may  be  thought  to  be  remnants  of 
old  valvular  lesions.  The  differentiation  from  typhoid  fever  on  the  one 
hand  and  acute  miliary  tuberculosis  on  the  other  may  be  impossible  by 
the  simple  methods  of  physical  diagnosis,  and  the  diagnosis  must  rest  with 
the  blood  culture.  Occasionally  the  presence  of  petechiae  in  the  skin  may 
suggest  typhus  fever.  Examination  of  the  eye-grounds  may  show  small 
white  spots  of  retinal  exudation  and  occasional  hemorrhages,  but  the  pic- 
ture may  be  difficult  to  distinguish  from  typhoid  lymphomata  or  miliary 
tubercles.  The  presence  of  leucocytosis  is  suggestive,  but  not  decisive, 
while  the  absence  of  Widal  reaction  is  of  value  only  as  negative  evidence. 
The  only  decisive  evidence  is  given  by  the  blood  culture. 

Cerebral  Type. — In  the  third  or  cerebral  type  the  symptoms  due  to 
embolism  of  the  brain  and  usually  of  the  left  middle  cerebral  artery  domi- 
nate the  picture.  There  is  a  history  of  onset  with  fever,  weakness,  and 
perhaps  chills,  perhaps  a  shower  of  petechiae  over  the  body,  and  hsematuria, 
and  then  a  sudden  onset  of  hemiplegia,  with,  or  more  usually  without,  con- 
vulsions, and  perhaps  relapse  into  unconsciousness.  The  patient  is  then 
left  with  unconsciousness,  hemiplegia  (usuallj'  right-sided),  and  usually 
aphasia,  more  or  less  disturbance  of  vision,  and  choked  disk.  The  septic 
infarct  may  also  give  rise  to  purulent  meningitis,  so  that  there  may  be 
unconsciousness,  rigidity  of  the  neck,  and  Kernig's  sign  as  well,  and  the 
cerebrospinal  fluid  obtained  from  lumbar  puncture  may  be  under  high 
tension,  cloudy,  rich  in  albumen  and  in  cocci. 


ENDOCARDITIS.  309 

These  lesions  are  produced  by  septic  emboli  of  varying  sizes  carried 
off  the  necrotic  surfaces  of  the  infected  valves.  In  Border's  series  they 
occurred  in  14.6  per  cent,  of  the  cases.  The  symptoms  vary  in  character 
and  severity,  according  to  the  location  and  extent  of  the  lesion,  from  a  few 
choreiform  movements  to  paralyses,  convulsions,  and  coma.  Aphasia  is, 
of  course,  relatively  common. 

The  diagnosis  of  the  primary  condition  may  depend  upon  the  varying 
heart  signs  and  the  positive  blood  culture. 

CHRONIC   INFECTIVE    ENDOCARDITIS    (OSLER). 

Osier  has  called  attention  to  the  existence  of  a  chronic  form  of 
malignant  endocarditis,  which  may  last  from  four  to  fourteen 
months.  It  is  characterized  by  an  asthenic  condition,  with  remittent  or 
intermittent  fever  rising  to  a  maximum  of  102°-103°,  chills  and  sweats, 
in  about  60  per  cent,  of  the  cases,  petechias,  especially  upon  the  shins, 
enlarged  spleen,  and  heart  signs,  which  vary  as  the  process  extends  from 
valve  to  valve,  or  the  valve  substance  sloughs.  There  is  usually  a  progres- 
sive anaemia.  The  leucocytes  are  almost  always  increased  (10,000  to 
15,000  per  c.mm.),  though  not  so  greatly  as  in  the  acute  forms,  and  the 
blood  culture  is  usually  positive.  However,  in  this  condition  more  than  in 
any  other,  it  may  occur  that  a  single  blood  culture  may  be  negative, 
whereas  a  subsequent  attempt  may  give  a  good  growth,  for  the  germs  are 
apt  to  pass  into  the  blood  in  showers. 

In  Osier's  experience  the  disease  was  always  fatal,  but  Horder  reports 
one  case  with  recovery. 

DIAGNOSIS. 

The  diagnosis  of  malignant  endocarditis  often  presents  considerable 
difficulty.  The  differentiation  from  pneumonia  may  be  especially  difficult, 
since  there  are  usually  small  areas  of  septic  bronchopneumonia  present. 
On  the  other  hand,  as  Rosenow  has  shown,  the  blood  culture  in  pneu- 
monia often  yields  large  numbers  of  pneumococci,  and  this  germ  is  not 
infrequently  the  cause  of  malignant  endocarditis. 

Thompson  has  also  called  attention  to  the  fact  that  acute  hyperthyroidism  (Base- 
dow's disease,  exophthalmic  goitre)  may  present  a  clinical  picture  of  fever,  chills,  sweats, 
tachycardia,  dilated  heart  with  systolic  murmurs,  which  closely  simulates  that  of  malig- 
nant endocarditis.  The  thyroid  in  these  cases  is  enlarged  and  tender  and  the  ocular  signs 
are  usually  pronounced. 

The  crucial  points  in  the  differential  diagnosis  of  malignant  endocar- 
ditis are,  therefore,  given  in  the  following  table : 

From  penumonia — petechiae,  signs  of  valvular  lesions. 

From  typhoid  fever — by  leucocytosis,  absence  of  Widal  reaction,  blood  culture. 

From  rheumatic  fever — by  enlarged  spleen,  petechiae,  chills,  blood  culture. 

From  malaria — by  absence  of  plasmodia,  leucocytosis,  heart  signs,  positive  blood 

culture. 
From  miliary  tuberculosis — ^by  leucocytosis,  heart  signs,  absence  of  tubercle  bacilli, 

positive  blood  culture. 
From  cerebrospinal  meningitis — by  absence  of  intracellular  diplococci  in  cerebro- 
spinal fluid,  positive  blood  culture  yielding  other  germs. 
From  acute  Basedow's  disease — by  positive  blood  culture,  absence  of  oculomotor 
signs  of  Basedow's  disease,  polymorphonuclear  leucocytosis. 


310  DISEASES   OF   THE    HEART    AND    AORTA. 

Case  of  Malignant  Endocarditis. 

Margaret  P.,  aged  12,  factory  worker.  Previously  healthy  except  for  scarlatina  at 
5  years  and  measles  at  7.  Never  had  rheumatism  or  chorea.  Two  weeks  before  admission 
she  had  a  shaking  chill,  followed  by  fever  and  sweats.  She  has  felt 
weak,  nauseated,  has  vomited  every  day,  and  is  irrational  on  the  day  of  her  admission. 
Has  had  no  headache  nor  epistaxis. 

At  the  time  of  her  examination  by  Dr.  Cole  she  was  irrational,  chilly,  and  shivering. 
Her  color  was  a  dusky  pallor  with  slight  cyanosis.  Slight  enlargement  of  glands; 
lungs  clear  except  for  a  few  mucous  rales. 

Heart.  —  Apex  impulse  cannot  be  seen  or  felt.  Dulness  extends  7  cm.  to  the 
left  and  2  cm.  to  the  right  of  the  midline,  and  above  to  the  second  rib.  At  the  apex 
there  is  a  well-marked  systolic  murmur,  transmitted  as  far  as  the  anterior  axil- 
lary line.     Pulse   is   regular,   of  fair   volume,    10  8   per  minute. 

The  border  of  spleen  is  just  felt.  Liver  dulness  extends  to  the  costal  margin. 
Reflexes:  Knee-jerks  active;  no  Kernig's  sign.  Rectal  examination  negative.  Vaginal 
smear  shows  no  intracellular  diplococci.  Blood  count,  Nov.  4.  Red  blood- 
corpuscles   4,352,000.     Haemoglobin   80   per  cent.     Leucocytes   31,460. 

The  maximal  blood-pressure  ranged  between  80  and  105  mm.  Hg;  the 
pulse-rate  between  120  and  210.  Differential  count  showed  polymorphonuclear 
9  6  . 4  per  cent.;  large  mononuclears  1.2  per  cent.;  small  lymphocytes  2.2  percent.  No 
malaria  parasites  in  the  blood.     Widal  and  blood  cultures  persistently  negative. 

The  patient's  general  condition  remained  about  the  same.  On  Nov.  6  a  few  e  c  - 
chymoses  appeared  on  the  back  and  abdomen.  By  Nov.  7  the  systolic  murmur  was 
well  heard  in  the  axilla.  Lumbar  puncture  gave  a  clear  sterile  fluid  under  pressure 
of  280  mm.  (slightly  elevated).  Nov.  12.  A  few  pin-point  vesicles  appeared  on  the 
abdomen,  along  with  new  petechiae  on  abdomen  and  face.  Nov.  14.  Patient 
better  and  temperature  lower.  Nov.  22.  Had  a  severe  shaking  chill;  slight  epistaxis. 
Nov.  26.  Felt  faint  while  in  the  tub.  Nov.  28.  Haemoglobin  65  per  cent.  Nov. 
29.  Cardiac  dulness  has  increased,  extending  9.5  cm.  to  the  left  and  4  cm. 
to  the  right;  above  to  the  second  left  interspace.  The  murmur  is  about  as  before;  the  pulse 
large  and  collapsing.  Dec.  1.  Anaemia  has  increased.  Red  blood-corpuscles 
3,800,000;  haemoglobin  60  per  cent.;  leucocytes  27,000.  Dec.  4.  A  well-marked  pre- 
systolic thrill  is  felt  at  the  apex.  In  the  afternoon  she  complained  of  pain  in  the 
feet  and  loss  of  sensation  in  feet  and  legs.  She  cannot  feel  touch  below  the 
knees.  The  feet  are  warm;  no  discoloration;  knee-jerl«  are  present.  Dec.  5.  Red  blood- 
corpuscles  2,300,000;  haemoglobin  50  per  cent.;  leucocytes  31,000.  The  pa- 
tient's condition  became  worse  and  crops  of  petechiae  appeared.  'The  pulse  became  irreg- 
ular in  force  and  rhythm.     She  died  on  Dec.  16. 

Autopsy  by  Dr.  MacCallum  showed  acute  vegetative  endocarditis 
of  the  mitral  valve,  cardiac  hypertrophy,  oedema  of  the  lungs,  acute  splenic  tumor 
with  anaemic  infarction,  acute  diffuse  nephritis  with  anaemic  infarction,  embolic  occlusion 
of  the  aorta  at  its  bifurcation.  A  motile  coccus  (micrococcus  rubescens)  was  found  in 
the  heart;  micrococcus  albus  and  bacillus  pseudodiphtheriae  in  the  vegetations;  and  in  the 
kidney  an  unidentified  actinomyces,  sarcina  flava^  and  micrococcus  albus. 

TREATMENT. 

The  treatment  of  malignant  endocarditis  is  the  treatment  of 
any  form  of  general  septicsemia, — absolute  rest,  very  light,  soft  or  milk 
diet  amounting  to  as  near  3000  calories  per  day  as  possible,  and  avoidance 
of  excitement.  Drugs  are  of  little  value.  Strychnine  may  be  given  in 
doses  of  2-3  mg.  (^V  to  yV  gr-)  every  four  hours,  or  digitalis  also,  with  a  view 
of  increasing  the  activity  of  the  vasomotor  centre  and  the  tonicity  of  the 
heart;  but  little  is  accomplished  by  their  use,  and  in  some  cases  the  heart 
muscle  is  already  so  much  injured  by  the  infection  that  further  stimu- 
lation is  actually  harmful.     Salt  infusions  may  be  given,  but  they  serve  to 


ENDOCARDITIS.  311 

swell  the  volume  of  blood,  to  dilate  the  heart,  and  to  increase  its  work, 
and,  although  they  may  perhaps  "  wash  out  the  toxic  substances  through 
the  kidneys,"  it  is  doubtful  whether  they  are  at  all  effectual. 

Intravenous  Injections. — Intravenous  infusions  of  collargol  and  other  metallic  com- 
pounds have  been  tried  and  some  apparently  favorable  results  reported,  but  these  have 
invariably  been  shown  to  be  overestimated  when  the  work  was  repeated  by  more  careful 
observers.  The  antistreptococcus  serum  of  Marmorek  has  been  used  in  cases  of  malignant 
streptococcic  endocarditis,  but  this  also  has  no  value. 

Inoculations  with  Bacterial  Vaccines. — More  recently  A.  E.  Wright  has  instituted 
the  method  of  inoculating  the  patient  with  small  doses  of  killed  cultures  of  the  germ,  caus- 
ing the  infection  in  the  hope  of  thereby  increasing  the  production  of  protective  substances. 
Though  this  is  the  most  promising  of  all  the  methods,  it  has  failed  to  give  satisfactory 
results  in  the  hands  of  careful  observers  such  as  Rosenow  and  Horder. 

SIMPLE   ACUTE   ENDOCARDITIS. 

The  malignant  forms  of  carditis  described  in  the  foregoing  chapter 
are  relatively  infrequent  (0.19  per  cent,  of  admissions  to  the  Johns  Hopkins 
Hospital).  Much  more  common  are  the  milder  infections  which  assume 
the  form  of  simple  acute  or  subacute  endocarditis,  and  in  which  the  symp- 
toms are  often  referable  mainly  to  a  mild  subacute  fever  and  anaemia,  and 
with  comparatively  less  frequency  stamped  with  the  typical  features  of  heart 
disease,  so  that  the  latter  may  become  evident  only  on  physical  examination. 

Rheumatism. — Like  the  malignant  form,  which  is  usually  of  pyogenic 
origin,  the  simple  endocarditis  is  far  more  frequently  rheumatic  (Bouillaud, 
1835),  manifesting  itself  in  association  with  other  manifestations  of  the 
"rheumatic  cycle," — tonsillitis,  rheumatic  arthritis,  chorea,  pleurisy,  or 
the  rheumatic  erythemata;  rheumatism  being  the  etiological  factor  in  65.6 
per  cent,  of  all  cases  of  endocarditis  in  the  Medical  Clinic  at  Zurich,  in  36.7 
per  cent,  at  Jena,  and  in  58  per  cent,  at  Leipzig. 

Similar  figures  appear  from  the  clinics  of  Great  Britain  and  America,  the  statistics 
of  the  Johns  Hopkins  Hospital  being  quite  according  to  the  rule. 

A  much  higher  percentage  of  the  cases  of  rheumatism  acquire  endocarditis  than  is 
true  of  any  other  disease.  It  was  present  in  61. .3  per  cent,  of  all  cases  of  this  disease  in 
children  in  West's  series,  in  66  per  cent,  of  Fuller's  cases  and  in  80  per  cent,  of  the  cases 
reported  by  Cadet  de  Gassicourt. 

Gibson  states  that  the  likelihood  of  endocardial  infec- 
tion is  proportional  to  the  severity  of  the  rheuma- 
tic   affection . 

The  same  relative  frequency  applies  also  to  chorea,  the  other  important  member  of 
the  rheumatic  cycle.  Stephen  Mackenzie  finds  60.6  per  cent.,  Donkin  40  per  cent.,  Osier 
51.4  per  cent.,  affected  with  carditis,  although  the  arthritic  history  is  often  absent. 

Other  Infections. — Other  diseases,  though  occasional  causes,  are  much  less  frequently 
followed  by  endocarditis.  Thus,  Osier  found  it  twelve  times  in  216  autopsies  upon  cases 
of  phthisis,  five  times  in  100  pneumonia  cases,  twice  in  80  autopsies  upon 
typhoid  fever;  and  he  states  that  it  is  not  uncommon  in  scarlet  fever. 
In  most  of  these  cases  the  secondary  infection  with  streptococcus  is  probably  responsible 
for  the  condition.  Influenza,  smallpox,  measles,  and  diphtheria  also 
are  occasional  etiological  factors.  In  all  these  diseases  any  overwork  or 
other  overstrain  upon  the  heart  during  the  course  of  the  in- 
fection increases  its  susceptibility  and  enhances  the  liability  to  affection 
of  the  endocardium,  just  as,  according  to  Poynton,  fright  (or  hard  study  at  school)  pre- 
disposes to  affection  of  the  brain,  namely  chorea. 


312 


diseasp:s  of  the  heart  and  aorta. 


Age. — As  to  age  it  may  be  said,  that,  in  contrast  to  both  the  malignant 
and  the  chronic  forms  of  endocarditis,  the  simple  acute  carditis  which  repre- 
sents the  usual  beginning  of  the  process  presents  itself  most  frequently  in 
children,  especially  in  the  second  decade  of  life,  and  that  the  age  of  maxi- 
mum frequency  is  the  age  of  the  greatest  expo- 
sure, the  second  and  third  decades. 

The  frequency  is  due  merely  to  the  fact  that  rheu- 
matism is  then  more  frequent,  although  when  contracted 
in  childhood  it  appears  to  be  followed  by  a  greater  per- 
centage of  cardiac  complications  than  in  older  persons, 
and  pericarditis  (especially  adherent  pericardium)  and 
myocarditis  are  more  severe.  Of  145  cases  under  15 
years  of  age  Holt  and  Crondall  found  under  5  years  14 
cases,  5-10  years  71  cases,  and  10-14  years  60  cases, 
38  per  cent,  being  males  and  52  per  cent,  females.  It 
is  especially  noteworthy  that  of  these  145  cases  almost 
90  per  cent,  were  brought  about  by  diseases  of  the  rheu- 
matic cycle,  in  contrast  to  60-65  per  cent,  in  older  persons. 
Indeed,  the  earlier  in  life  the  rheumatic  infection  is  con- 
tracted, the  more  it  assumes  the  type  of  a  general  carditis 
and  the  less  severely  are  the  joints  involved.  As  many 
writers  have  stated,  rheumatic  fever  in  children  usually  assumes  the  form  of  a  tonsillitis, 
with  carditis  and  chorea,  and  is  frequently  devoid  of  any  arthritic  symptoms  whatever. 
The  myocarditis  has  been  discussed  in  Part  II,  Chapter  IX,  and  is  an  important  fea- 
ture. The  weakness  of  the  heart  muscle  which  results  leads  to  dilatation  and  overfilling 
of  the  chambers,  and  this  in  turn  increases  the  leaks  due  to  the  lesions  upon  the  valves. 


Age 

-9 

-19 

-29 

-39 

■A3 

-59 

-69 

ftrHille 
40 

30 

A 

20 

M5- 

'       ^' 

y: 

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V 

10 

/ 

f^ 

J,. 

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0 

^ 

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-Al 

^^ 

Fig.  178.  —  Diagram  showing 
relative  frequency  of  the  most  im- 
portant valvular  lesions  at  various 
ages.  (Modified  from  Gillespie.) 
Solid  line,  mitral  insuflSciency;  bro- 
ken line,  mitral  stenosis;  dotted  line, 
aortic  insufficiency.  The  figures  in- 
dicate the  decades.  Under  9  years 
—9;  10-19,-19;  20-29,-29;  etc. 


Per  MITRAL         . 

Cent    iNSUFFiClENCVrj 

lOOf  


MITRAL 
STEN0513 


AORTIC  IN5UFFiaENCY^T°'^5|5 


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■■  CA5E5     J.H.H 

g=J  AUT0PSIE5  -BERL. 
Fig.  179. — Diagram  showing  the  relative  frequency  of  the  various  valvular  lesions  in  1781  cases  of 
valvular  heart  disease  admitted   to  the  Medical  Service  of   the  Johns  Hopkins  Hospital  from   1889  to 
1908,  as  well  as  those  found  by  Sperling  in  300  autopsies  in  Berlin.     Small  space,  5  per  cent.;  Berl.,  Berlin; 
J.  H.  H.,  Johns  Hopkins  Hospital. 

Sex.— Many  authors,  among  them  Osier,  state  that  men  are  more  fre- 
quently affected  than  women;  though  v.  Jurgensen  states  that  valvular 
disease  occurs  with  practically  the  same  frequency  in  both  sexes. 


INVOLVEMENT    OP    INDIVIDUAL    VALVES. 

The  relative  frequency  with  which  the  valves  are  involved  is  shown 
by  the  analysis  of  1781  cases  of  endocarditis  admitted  in  the  Johns  Hopkins 
Hospital  from  1889  to  1908,  represented  diagrammatically  in  Fig.  179. 
The  figures  show  a  general  correspondence  to  those  of  v.  Jurgensen  in  2470 
cases  in  the  German  clinics. 


ENDOCARDITIS.  313 


PATHOLOGICAL    PHYSIOLOGY. 

The  pathological  physiology  of  simple  acute  endocarditis  presents  the 
condition  due  to  the  individual  valvular  lesion  (to  be  considered  in  detail 
in  the  appropriate  chapters  dealing  with  the  chronic  endocarditis),  modi- 
fied or  added  to  by  an  element  of  diminished  vasomotor  tone  due  to  the 
acute  febrile  condition.  As  the  result  of  this  vasodilatation,  especially  in 
the  abdominal  area,  the  blood  collects  in  the  dilated  veins  and  capillaries, 
the  blood-pressure  may  be  low,  and  the  symptom  complex  of  arterial 
anaemia  or  low  blood-pressure  sets  in.  Moreover,  there  is  usually  a  certain 
degree  of  actual  anaemia  added  to  the  lesion,  and  this  often  increases  the 
difficulty  in  breathing;  although  it  does  not,  as  a  rule,  bring  on  the  red  and 
purple  hue  of  chronic  cyanosis.  Still  further  the  increase  in  the  leakage 
causes  damming  back  and  secondary  dilatation  of  the  chambers  behind 
it,  Cfidema  in  the  walls  of  the  ventricles  and  in  the  valve  cusps,  and 
increased  susceptibihty  to  infection. 

PATHOLOGICAL    ANATOMY. 

The  endocarditis  itself  is  less  severe  than  in  the  malignant  form.  Fewer 
bacteria  are  deposited  upon  the  valves,  and  these  show  less  tendency  to 
multiply,  so  that  the  process  of  organization,  as  a  rule,  outraces  necrosis, 
and  consequently  the  separation  of  emboli  is  rare.  The  valves  thus  show 
an  injured  surface  covered  by  a  more  or  less  thick  or  exuberant  layer  of 
fibrin,  with  active  organization  proceeding  upward  from  its  base.  This 
may  be  seen  in  any  stage  of  advancement,  from  fresh  fibrin  in  the  early 
stage  to  completely  organized  firm  young  connective  tissue,  covered  by 
intact  endothelium,  when  healing  has  become  complete. 

Pathologically,  the  difference  between  the  malignant  and  the  simple 
endocarditis  is  merely  the  usual  difference  between  a  mild  and  a  virulent 
infection  of  any  tissue.  There  may  be  no  actual  difference  in  etiology,  and 
the  malignant  form  may  represent  only  a  very  virulent  strain  of  the  same 
organism  which  would  ordinarily  produce  a  milder  infection;  or,  on  the 
other  hand,  micro-organisms  of  the  same  virulence  may  produce  different 
types  of  lesion  in  persons  with  different  powers  of  resistance. 

SYMPTOMS. 

It  is  particularly  noticeable  that  in  these  cases  during  the  first  attack 
the  symptoms  due  to  distinct  heart  failure  are  largely  absent,  and  the 
main  symptoms  are  those  of  accompanying  rheu- 
matic disease,  along  with  the  weakness,  pallor,  and  anaemia  (usually  about 
60  per  cent,  haemoglobin),  such  as  might  be  due  to  any  mild  fever,  though 
occasionally,  as  in  the  case  of  J.  A.  (page  316),  the  onset  of  aortic  insuffi- 
ciency is  attended  by  pain  and  sudden  collapse.  The  temperature  rarely 
attains  101°  unless  an  acute  arthritis  or  acute  pneumonia  is  present.  The 
pulse  is  usually  rapid  and  regular.  Its  quality  depends  upon  the  nature 
of  the  lesion,  being  large  and  collapsing  in  the  presence  of  aortic  insuffi- 
ciency, small  in  mitral  stenosis,  and  of  moderate  size  in  mitral  insufficiency. 
The  blood-pressure  is  sometimes  above,  sometimes  below  normal. 


314  DISEASES   OF   THE   HEART   AND   AORTA. 


PHYSICAL   SIGNS. 

As  a  rule,  the  patient  does  not  seem  very  ill,  he  has  sometimes  an 
anxious  expression,  is  usually  pale  and  sallow,  in  contrast  to  the 
older  cases  of  mitral  disease,  who  usually  show  a  flushed  and  cyanotic  hue. 
Occasionally  choreic  movements  are  present.  It  is  very  common  for  the 
tonsils  to  be  enlarged,  since  these  are  the  usual  portals  of  entry  for  the 
rheumatic  infection,  and  there  is  frequently  a  yellow  exudate  in  the  crypts 
or  a  membrane  over  their  surfaces.  In  almost  all  rheumatic  cases  there 
are  foci  of  cocci  (streptococcus  or  micrococcus  rheumaticus?)  in  the  deeper 
tissue  of  the  tonsil.  Along  with  this  infection  the  so-called  tonsillar  lymph 
gland  just  below  the  angle  of  the  jaw  and  often  the  submaxillar^'^  and 
anterior  cervical  lymph  glands  are  enlarged.  The  chest  shows  no  special 
pecuUarity  except  that  precordial  bulging  is  often  present,  espe- 
cially marked  in  children  (see  page  88),  even  in  the  first  attack  of  endo- 
carditis. The  cardiac  signs  are  the  same  as  for  the  chronic  valvular  lesions, 
though  usually  less  marked.  They  will  be  discussed  in  detail  under  the 
special  chapters. 

The  liver  is  usually  not  enlarged  unless  there  is  marked  heart  fail- 
ure. Occasionally  the  spleen  is  palpable  and  even  hard,  tender,  and 
painful,  as  a  result  of  a  fresh  or  old  infarct,  and  this  condition  may  persist 
unchanged  for  years. 

A  few  months  ago  the  writer  saw  in  the  Johas  Hopkins  Dispensary  a  young  girl  in 
whom  a  large,  very  hard  spleen  had  been  present  for  several  years,  first  appearing  during 
a  rather  severe  attack  of  simple  acute  mitral  endocarditis. 

There  is  often  slight  oedema  of  feet  and  ankles,  though  very  many 
cases  come  to  treatment  before  this  has  set  in.  The  presence  of  oedema 
in  an  early  acute  endocarditis  is  a  rather  grave  sign,  since  it  indicates  the 
failure  of  the  heart  to  respond  promptly  to  the  added  load. 

The  urine  is  usually  of  high  specific  gravity  and  contains  a  small 
amount  of  albumen  and  a  few  coarsely  or  finely  granular  casts, — a  typical 
febrile  albuminuria. 

The  blood  examination  usually  shows  a  slight  grade  of  secondary 
anaemia. 

SUBSEQUENT    COURSE. 

As  in  the  cases  cited  on  page  316,  there  is  usually  gradual  improve- 
ment under  any  treatment  in  which  the  main  factor  is  sufficient  rest, 
during  which  the  infection  subsides  (the  bacteria  dying,  or  more  commonly 
becoming  latent),  the  vegetations  undergo  gradual  organization  and  more 
or  less  thickening  or  shrinkage,  and  fever  passes  off,  as  does  the  acute  myo- 
cardial weakness.  The  patients  almost  always  recover  from  the  first  attack. 
Recurrence  is  especially  common,  and  is  the  danger  against  which  especial 
precaution  must  be  taken,  the  more  so  as  the  second  attack  often  spreads 
to  another  valve  or  even  to  two  more.  It  is  the  liability  to  repeated  attacks 
which  keeps  the  pathological  process  ever  fresh  and  increasing.  There  is 
then  usually  a  little  area  of  incompletely  organized  fibrin  always  present 
to  give  soil  to  any  stray  micrococcus  that  may  be  carried  by  the  blood 
stream,  and  thus  produce  a  new  outbreak  of  fresh  endocarditis  with  exacer- 
bation and  perpetuation  of  the  old  symptoms.     After  a  single  attack, 


ENDOCARDITIS.  315 

especially  when  one  only  is  involved,  complete  organization  of  the  vegeta- 
tion may  set  in,  the  acute  myocardial  changes  subside,  and  the  heart  muscle 
may  soon  regain  its  normal  function. 

Compensation. — A  slight  leak  (see  page  322)  may  remain  at  the  site 
of  the  vegetation,  just  enough  to  produce  a  murmur  and  perhaps  even 
bring  about  slight  hypertrophy,  but  without  really  impairing  the  function 
of  the  heart;  and  the  individual  who  suffers  from  no  further  acute  endo- 
cardial changes  may  go  on  for  thirty  or  forty  years,  until  the  age  of  sclerosis 
sets  in  and  the  leak  is  widened  by  sclerotic  shrinkage,  without  the  appear- 
ance of  any  further  symptoms.  On  the  other  hand,  as  da  Costa  has  shown, 
persons  with  old  perfectly  compensated  valvular  lesions  are  much  more 
susceptible  to  cardiac  overstrain  and  acute  dilatation  than  are  normal 
individuals.  With  the  dilatation  there  comes  a  functional  insufficiency 
of  the  valves,  which  adds  its  effect  to  that  of  the  organic  lesion;  and  finally, 
as  Roy  and  Adami  have  shown,  stasis  brings  about  oedema  and  cellular 
infiltration  in  the  cusps.  This  infiltration  is  followed  by  further  valvular 
sclerosis  and  shrinking,  and  thus  the  cardiac  overstrain  in  itself  tends  to 
increase  permanently  the  original  lesion. 

When  hypertrophy  and  compensation  are  good  and  the  individual 
either  lives  a  quiet  life  or  has  developed  his  muscles  gradually  to  meet  the 
strain  of  his  surroundings,  he  may  escape  overstrains  entirely,  and  the 
lesion  may  either  be  stationary  or  may  shrink  by  gradual  sclerosis.  It  is 
a  rather  common  occurrence  to  find  perfectly  healthy  young  adults  or  even 
active  men  in  middle  age  who  have  had  well-compensated  mitral  insuffi- 
ciency persent  since  childhood.  The  same  is  also  true  of  aortic  insuffici- 
ency except  that  this  usually  again  makes  itself  felt  about  the  age  of  arterio- 
sclerosis, i.e.  about  the  age  of  forty.  Even  then,  with  good  care,  general 
hygiene,  avoidance  of  muscular  overstrain,  nervous  excitement,  and  over- 
eating,  great  moderation  in  the  use  of  alcohol  and  tobacco,  and  especially 
personal  prophylactic  measures  against  infectious  diseases,  a  long  life 
may  be  attained  by  the  patient. 

Reinfection. — On  the  other  hand,  when  the  patient  is  still  subject  to 
recurrence  of  his  rheumatism  or  tonsillitis,  or  to  repeated  attacks  of  pneu- 
monia, bronchitis,  or  influenza,  the  probability  that  the  cardiac  lesion  will 
remain  quiescent  is  a  small  one,  and  it  becomes  more  likely  that  both  valve 
and  muscle  will  suffer  further  changes  whose  limit  it  is  impossible  to  pre- 
dict. It  is  therefore  most  important  not  to  give  a  definite  prognosis  to  the 
family  or  friends  of  the  patient  until  he  has  been  under  observation  for  about 
a  year  after  the  attack  of  endocarditis  has  subsided,  so  that  all  these  factors 
may  be  carefully  watched  and  taken  into  account,  prophylactic  measures 
be  instituted,  and  the  recuperative  power  of  the  heart  muscle  be  gauged. 

Complications. — Another  factor  even  more  important  than  the  endo- 
cardial lesion  is  the  involvement  of  the  pericardium  and 
especially  the  production  of  adherent  pericardium,  so  common 
in  the  first, and  second  decades.  This  condition  perhaps  more  than  any 
other  leads  to  early  heart  failure,  since  it  imposes  the  greatest  strain  of  all 
upon  the  heart;  and,  as  it  develops  insidiously  and  frequently  reaches  its 
maximum  only  after  the  first  acute  attack  has  passed  off,  it  should  be 
watched  for  with  great  care. 


316  DISEASES   OF   THE   HEART   AND    AORTA. 

SIMPLE    ACUTE    ENDOCARDITIS. 

J.  A.,  male,  cannery  worker,  aged  15,  entered  the  hospital  complaining  of  rheu- 
matism. He  has  been  a  rather  dehcate  boy,  having  had  erysipelas,  measles,  whooping- 
cough,  and  chicken-pox  when  a  child,  and  attacks  of  definite  articular  rheumatism  at  nine 
and  ten  years.    He  has  done  soldc-ring  in  a  cannery  for  the  past  two  years. 

About  five  weeks  before  admission  he  began  to  complain  of  p  a  i  n  in  h  i  s 
ankles  and  knees,  for  which  he  was  put  to  bed.  At  this  time  his  physician  found 
a  temperature  of  104°,  and  he  had  chilly  sensations,  but  no  shaking  chills. 
About  two  weeks  later  while  lying  down  he  felt  an  intense  pain  in  his  heart  and  be- 
gan to  get  white  in  the  face  and  blue  at  the  lips.  Since  then,  though  he  has  been 
losing  weight  and  strength,  he  has  had  no  more  pain.  He  has  had  occasional  headaches 
during  the  illness. 

Examination  shows  a  well-nourished  boy  of  sallow  color,  with  injected  pharynx, 
enlarged  tonsils,  and  enlarged  posterior  cervical  and  axillary  lymph-glands.  Chest 
is  well  formed  and  lungs  are  negative  but  for  a  few  moist  rales  over  the  left  apex. 

Heart . — There  is  marked  precordial  bulging.  The  apex  beat  is  seen  in 
the  4th  left  interspace  9  cm.  from  the  midline.  Dulness  extends  4  cm.  to  the 
right  of  the  midline  and  above  to  the  second  rib.  There  are  no  thrills.  The  first 
sound  at  the  apex  is  preceded  by  a  short  rumble  (Flint  murmur)  and  replaced 
by  a  soft  blowing  systolic  murmur.  The  second  sound  is  clear  at  the  apex, 
but  at  and  near  the  sternum  is  followed  by  a  blowing  diastolic  murmur, 
maximum  over  the  insertion  of  the  third  right  rib.  The  pulse  is  124  per  minute, 
small  but  definitely  collapsing,  and  there  are  well-marked  capillary 
pulsation  and  throbbing  of  the  carotids.     Blood-pressure:  maximal  115-125  mm.  Hg. 

Joints.  — There  are  swelling  of  right  elbow  and  left  ankle  and 
soreness  of  elbows,  knees,  and  right  hip;  slight  wasting  of  interossei  of  hands  and  feet. 
Genitalia  and  reflexes  are  normal. 

There  is  no  oedema.  Red  blood-corpuscles  5,000,000;  haemoglobin  75  per  cent.; 
leucocytes  11,000.  Urine. — Lemon  yellow.  Specific  gravity  1015;  alkaline;  no 
sugar;  a  trace  of  albumen;  a  considerable  number  of  coarsely  granular  casts. 

Oct.  31.  Dulness  extends  7.5  cm.  to  the  left  of  the  midline  and  2.5  cm.  to 
the  right.  Nov.  13.  Red  blood-corpuscles  5,000,000;  haemoglobin  80  per  cent.;  leuco- 
cytes 6,600.  General  condition  is  excellent.  Pulse  continues  rapid.  The  joints  are  clear. 
Jan.  5.  There  has  been  gradual  progressive  improvement.  Red  blood-corpuscles  4,700,000; 
haemoglobin  90  per  cent.;  leucocytes  11,000.  There  has  been  a  gradual  rise  in  the  maximal 
pressure  to  1.50-160  mm.  Hg,  as  the  patient's  improvement  has  continued  in  spite  of  the 
rapid  pulse.  The  patient  was  discharged  quite  well  on  Jan.  17,  but  had  a  second  more 
severe  attack  several  years  later. 

TREATMENT. 

The  treatment  of  the  acute  attack  of  endocarditis  partakes  in  general 
of  the  treatment  of  a  mild  febrile  disease  or  a  secondary  anaemia  on  the 
one  hand,  and  of  the  particular  valvular  disease  on  the  other.  Rest  in 
bed  until  a  couple  of  weeks  after  the  subsidence  of  all  febrile  symptoms 
is  therefore  an  absolute  necessity,  also  light  and  easily  digestible  diet,  at 
first  of  800-1000  calories,  later  2500. 

Digitalis  and  Strychnine. — As  a  rule,  digitalis  is  not  absolutely 
necessary,  and  is  dispensed  with  by  most  Anglo-American  practitioners. 

However,  Cloetta  has  shown  that  the  hearts  of  animals  in  which  aortic  insufficiency 
has  been  produced  experimentally  recover  much  better,  undergo  much  less  dilatation,  and 
acquire  much  greater  strength  if  digitalis  treatment  is  begun  at  once  and  is  continued  over 
long  periods  (about  a  year)  than  if  this  treatment  is  omitted.  Cloetta  claims  equally  good 
results  in  man,  but  his  cases  are  too  few  to  warrant  conclusions.  Nevertheless,  the  results 
are  sufficiently  definite  to  warrant  the  prolonged  use  of  digitalis  in  small  doses  (0.3  to  0.6 
CO.;  "Iv  to  X  of  the  tincture)  in  cases  of  acute  endocarditis  with  cardiac  dilatation. 


ENDOCARDITIS.  317 

In  cases  in  which  digitalis  is  not  used  strychnine  should  be  given 
in  doses  of  2  to  3  mg.  (^V  to  ^V  g^-)  three  or  four  times  a  day. 

The  salicylate  preparations,  sodium  salicylate,  salol,  salipy- 
rin,  aspirin,  etc.,  should  be  given  for  the  rheumatism;  but,  although  they 
certainly  relieve  the  pain,  and  it  has  been  shown  that  they  are  excreted 
into  the  joint  cavity,  the  duration  of  the  fever  and  arthritis  does  not  seem 
to  be  much  affected  by  them,  and  certainly  the  frequency  of  cardiac 
involvement  is  unchanged.  On  the  other  hand,  the  salicylates,  especially 
in  large  doses,  have  a  depressant  effect  upon  the  heart,  and  the  use  of 
these  drugs  should  therefore  be  as  restricted  as  is  consistent  with  relief  of 
arthritic  pain. 

According  to  many  authorities,  the  salicylates  seem  to  be  more  effective  when  in- 
jected directly  into  the  joint  or  into  the  tissues  immediately  surrounding  it.  The  writer's 
experience  with  this  method  is  limited  and  in  the  cases  tried  its  results  were  not  striking, 
but  it  is  sometimes  worthy  of  trial.  Oil  of  wintergreen  (Oleum  gaultheriae,  methyl  sali- 
cylate) applied  to  the  skin  over  the  joint  also  seems  to  cause  great  relief  of  pain,  but  it  is 
possible  that  the  rubbing  may  also  cause  more  of  the  micrococci  to  be  thrown  out  in  the 
blood  stream  than  might  otherwise  be  the  case.  Hot  compresses  of  saturated  aqueous 
solutions  of  oil  of  wintergreen  to  the  joint  may  suffice  to  allay  pain. 

Other  Therapeutic  Measures. — It  is  most  important  to  relieve  anaemia, 
which  is  usually  present  and  which  is  always  a  contributing  factor  to  the 
fatty  degeneration  and  weakness  of  the  myocardium.  Rest,  full  diet 
especially  rich  in  eggs,  milk,  and  green  vegetables,  and  administration  of 
iron  usually  relieve  this  symptom. 

The  iron  may  be  administered  as  Pil.  ferri  carbonatis  (Blaud's  pills),  0.2  to  0.3  C. 
{gr.  iii  to  gr.  v)  t.i.d.,  p.c;  or  Massa  ferri  carbonatis  (Vallet's  mass,  a  more  stable  prepa- 
ration containing  honey  instead  of  sugar);  Elixir  ferri,  cjuininse  et  strychninae,  8  c.c.  (5ii) 
t.i.d.,  a.c;   or  as  Syrup,  ferri  iodid.,  1  c.c.  (ttv  xv)  t.i.d.,  p.c. 

If  the  anaemia  is  severe  or  does  not  yield  to  iron  alone,  arsenic  should 
be  given  as  well,  since  it  has  been  shown  that  iron  and  arsenic  together 
accelerate  formation  of  red  corpuscles  and  haemoglobin  more  than  does 
either  drug  alone. 

Arsenic  is  usually  given  in  the  form  of  Liquor  potassii  arsenitis  (Fowler's  solution), 
beginning  in  doses  of  0.2  c.c.  (TT^iii)  t.i.d.,  p.c,  and  increasing  one  drop  at  each  dose  until 
1  c.c.  (TT\,xv)  is  reached  or  puffy  eyelids  and  albuminous  urine  show  that  the  physiological 
limit  has  been  reached. 

Prophylactic  Treatment. — One  of  the  most  important  factors  in  hasten- 
ing the  healing  of  a  fresh  vegetation  is  to  keep  it  from  being  reinfected  by 
bacteria  floating  in  the  blood  stream.  Every  focus  of  infection  is  a  store- 
house from  which  a  few  bacteria  are  given  off  from  time  to  time,  and  hence 
is  a  source  of  danger.  Accordingly  in  a  number  of  clinics,  and  particularly 
in  the  medical  clinic  of  the  Johns  Hopkins  Hospital,  under  Prof.  Barker's 
direction,  an  effort  is  being  made  to  stamp  out  every  focus  of  infection  to  be 
found  anywhere  in  the  body.  Carious  teeth,  paronychias,  and  ischiorectal 
abscesses  are  removed.  Particular  attention  is  given  to  the  tonsils.  These 
organs  are  the  main  portals  of  entry  for  the  rheumatic  infection.  In  persons 
who  are  subject  to  recurrent  tonsillitis  there  are  almost  always  small  ab- 
scesses containing  cocci  persisting  in  the  depths  of  the  tonsillar  tissue,  even 
when  there  is  no  inflammation  visible  upon  the  surface.    These  are  perma- 


318  DISEASES   OF   THE   HEART    AND    AORTA. 

nent  portals  of  infection.  Dr.  Barker  therefore  insists  upon  the  removal 
of  enlarged  tonsils  in  most  cases  of  rheumatic  heart  disease.  This 
should  be  done  between  but  not  during  the  attacks,  since 
there  is  danger  of  throwing  more  cocci  into  the  blood.  The  improvement 
which  follows  removal  is  sometimes  immediate  and  striking.  The  patient's 
color  improves  within  a  few  days.  He  feels  better.  His  expression  is 
brighter,  and  he  appears  more  robust.  Improvement  is  more  rapid  and, 
since  reinfection  is  less  frequent,  it  is  more  permanent. 

It  is  naturally  of  great  importance  that  all  the  tonsillar  tissue  should  be  removed, 
since  a  small  amount  left  in  place  may  again  undergo  hypertrophy  and  become  reinfected. 
Such  complete  removal  is  impossible  with  the  guillotine,  the  snare,  and  the  electro-cautery, 
and  is  extremely  difficult  by  even  the  ordinary  intracapsular  dissection.  The  most  satis- 
f^tory  method  known  to  the  writer  is  the  extracapsular  dissection  as  performed  by  Bordley. 

Pallative  Treatment  of  the  Tonsils. — By  way  of  palliative  or  prophy- 
lactic treatment  various  antiseptic  gargles  may  be  used.  Gargles  which 
contain  hydrogen  peroxide  are  to  be  preferred,  because  the  pus-cells  con- 
tain a  catalase  which  sets  free  the  oxygen.  The  nascent  oxygen  is  a  power- 
ful antiseptic,  and  the  excess  collects  in  bubbles  which  mechanically  loosen 
and  sweep  off  the  exudate.  The  hydrogen  peroxide  should  not  be  stronger 
than  2  volume  per  cent,  (one  part  commercial  hydrogen  peroxide  to  four 
parts  of  water). 

Other  gargles  that  may  be  used  are  Dobell's  solution,  dilute  Lugol's 
solution,  and  dilute  potassium  chlorate  solution  (especially  with  equal 
parts  of  dilute  hydrogen  peroxide.) 

BIBLIOGRAPHY. 

Endocarditis. 

Bouillaud:  Traits  des  maladies  du  cceur,  Paris,  1835,  ii.    Quoted  from  Nothnagel's  System, 

"Diseases  of  the  Heart,"  transl.  by  G.  Dock,  Phila.,  1908. 
Lenhartz,  H. :  Die  septische  Erkrankungen,  Nothnagel's  Handb.  d.  spec.  Pathol,  u.  Therap., 

iii,  2te  Theil,  Wien,  1904. 
Vieussens.    Quoted  from  C.  Hilton  Fagge,  "Diseases  of  the  Valves  of  the  Heart,"  Rey- 
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are  quoted. 
Hunter,  John:  Catalogue  of  Pathological  Specimens,  iii,  197. 
Meckel:  Mem.  de  I'Acad.  Roy.  des  Sciences,  Berl.,  1756.    Quoted  from  Friedreich,  "Krank- 

heiten  des  Herzens,"  Virchow's  Handb.  d.  spez.  Pathol,  u.  Therap.,  1867. 
De  Senac,  J.:  Traits  de  la  structure  du  cceur,  de  son  action  et  de  ses  maladies,  Par.,  1749. 
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Paris,  1806. 
Bums,  Allan:  Observations  on  some  of  the  Most  Frequent  and  Important  Diseases  of  the 

Heart,  Edinb.,  1809. 
Kreysig:  Die  Krankheiten  des  Herzens,  Berlin,  1815. 
Virchow,   R.:  Ueber  die   Chlorose  und  die  damit   zusammenhangenden   Anomalien  im 

Gefass-Apparate  insbesondere  ueber  Endocarditis  puerperalis,  Berl.,  1872. 
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V.  Langer,  L.:  Ueber  die  Blutgefasse  in  den  Herzklappen  bei  Endocarditis  valvularis. 

Arch.  f.  path.  Anat.,  etc.,  Berl.,  1887,  cix,  465. 
Darier,  J.:  Les  vaisseaux  des  valvules  du  cceur  chez  I'homme  a  I'^tat  normale  et  k  I'^tat 

pathologique.  Arch,  de  physiol.  norm,  et  path..  Par.,  1888,  4  s^r.,  ii,  35,  151. 
Winge.     Quoted  by  H.  Heiberg,  Ein  Fall  von  Endocarditis  ulcerosa  puerperalis  mit  Pilz- 

bildungen  im  Herzen  (Mycosis  Endocardii),  Arch.  f.  path.  Anat.,  etc.,  Berl.,  1872, 

Ivi,  407. 


ENDOCARDITIS.  319 

Weichselbaum :  Zue  jEtiologie  der  akuten  Endocarditis,  Centralb.  f.  feakteriol.  u.  Para- 

sitenk,  Jena,  1887,  ii,  209. 
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Leipz.,  1878,  ix,  1;   and  Lehrb.  d.  Herzkrankheiten,  Berl. 
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1886,  ciii,  333. 
Orth,  J.:  Ueber  die  ^tiologie  der  experimentellen  mycotischen  Endocarditis  Nachschrift 

zur  vorstehenden  Mittheilimg  des  Dr.  Wyssokowitsch,  ibid.,  p.  332. 
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Leipz.,  1885,  and  Fortschr.  d.  Med.,  Berl.,  1886,  iv,  1. 
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Wyler,  M.:  Ueber  einen  Fall  von  Endokarditis  recurrens.  Inn.  Diss.,  Zurich,  1897. 
Prudden,  T.   M.:  Experimental  Mycotic  or  Malignant   Ulcerative  Endocarditis,  Trans. 

Ass.  Am.  Physicians,  Phila.,  1886,  i,  207. 
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Hopkins  Hosp.,  Baltimore,  1907,  xviii. 
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Endocarditis,  J.  Infect.  Dis.,  Chicago,  1909,  vi,  245. 
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Practice,  transl.  by  G.  Dock,  Phila.,  1908. 
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xix,  909;    also,  Michaelis,  M.:  Zur  Endocarditis  gonorrhoica,  ibid.,  1893,  xix,  1123. 
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blenorrhagique.  Arch,  de  M^d.  exper.  et  d'Anatomie  pathol.,  Paris,  vii,  701,  and  Johns 

Hopkins  Hosp.  Bull.,  Bait.,  1896,  vii,  57. 
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de  Med.,  1899,  iii,  5  sec.  350. 
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J.  Exper.  M.,  N.  Y.,  1899,  iv,  81. 
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Phila.,  1905,  xx,  391. 
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of  the  Gonococcus,  Am.  J.  M.  Sci.,  Phila.,  1901. 
V.  Hofmann,  K.  Ritter,  Gonorrhoische  allgemein  Infektion  und  Metastasen,  Centralb. 

f.  d.  Grenzgeb.  d.  Med.  u.  Chir.,  1903,  vi,  308.     (Complete  review  of  the  literature  up 

to  that  date.) 
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Horder,  T.  J.:  Infective  Endocarditis,  Quart.  M.  J.,  Oxford,  1909,  ii,  289. 
Sahli,  H.:  Zur  ^tiologie  des  acuten  Gelenkrheumatismus,  Deutsch.  Arch.  f.  klin.  Med., 

1893,  H,  451. 
Dana:  Microbic  Origin  of  Chorea,  Am.  J.  M.  Sci.,  Phila.,  1894,  cvii,  31. 
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med..  Par.,  1898,  xviii,  189. 
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menhang  von  acuten  Gelenkrheumatismus  und  chorea,  Berl.  klin.  Wchnschr.,  1899, 

xxxvi,  638. 
Poynton,  F.  J.,  and  Paine,  A.:  The  Etiology  of  Rheumatic  Fever,  Lancet,  Lond.,  1900, 

ii,  861.    Also  Some  Further  Observations  upon  Rheumatic  Fever,  ibid.,  1901,  i,  1260. 

The  Present  Position  of  the  Bacteriology  of  Rheumatic  Fever,  Brit.  M.  J.,  Lond., 

1901,  ii,  779.     The  Pathology  of  Rheumatism,  Practitioner,  Lond.,   1901,  Ixvi,  22. 

Arthritis:  A  Comment  upon  and  Review  of  some  Recent  Literature  upon  the  Subject, 

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Acute  Rheimiatic  Fever,  International  Clin.,  Phila.,  1904,  ser.  xiii,  vol.  iv,  95.    Re- 


320  DISEASES   OF   THE   HEART   AND    AORTA. 

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A  Review  and  Study  of  some  Recent  Writings  upon  Arthritis  and  Ivindred  Disorders, 

Practitioner,  Lond.,   1904,  Ixxii,  864.     A  Lecture  on  Combined  Aortic  and  Mitral 

Disease  in  Rheumatic  Children,  Brit.  M.  J.,  Lond.,  1905,  ii,  837.    Observations  upon 

Arthritis  in  Young  Children,  Edinb.  M.  J.,  1907,  xxii,  226. 
Meyer,  F.:  Zur  Bakteriologie  des  akuten  Gelenkrheumatismus,  Deutsch.  med.  Wchnschr., 

Leipz.,  1901,  xxvii,  81. 
Singer,  G.:  Weitere  Erfahrungen  ueber  die  JEtiologie  des  acuten  Gelenkrheumatismus, 

Wien.  klin.  Wchnschr.,  1901,  xiv,  482. 
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Leipz.,  1903,  Ixxvi,  150. 
Walker,  E.  W.  A.:  On  the  Micrococcus  of  Acute  Rheimiatism,  Practitioner,  Lond.,  1903, 

Ixx,  185. 
Beaton,  R.  M.,  and  Walker,  E.  W.  A.:  The  Etiology  of  Acute  Rheimiatism  and  Allied 

Conditions,  Brit.  M.  J..  Lond.,  1903,  i,  237. 
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Lond.,  1903-04,  ix,  158. 
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ix,  272. 
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Articular  Rheumatism,  J.  Infect.  Dis.,  Chicago,  1904,  i,  714.    The  Etiology  of  Acute 

Articular  Rheumatism,  N.  York  and  Phila.  M.  J.,  N.  York,  1906,  Ixxxiii,  534. 
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Isolated  from  the  Blood  of  a  Ca.se  of  Rheumatism,  Endocarditis,  and  Chorea,  Am. 

J.  M.  Sc.,  Phila.,  1904,  cxxviii,  601. 
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Johns  Hopkins  Hosp.  Bull.,  Bait.,  1899,  x,  194. 
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Practice  of  Medicine,  J.  Am.  M.  Ass.,  Chicago,  1908,  li,  473. 
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klin.  Med.,  Leipz.,  1899,  Ixiv,  763. 
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Holt  and  Crondall.     Quoted  from  Horder. 
Barker,  L.  F.:  Clinical  Lectures  at  the  Johns  Hopkins  Hospital.     (Unpublished.) 


II. 

MITRAL  INSUFFICIENCY. 

OCCURRENCE. 

Of  all  the  valvular  lesions  those  involving  the  mitral  valve  are  the 
most  common,  especially  those  which  lead  to  the  production  of  a  leak  at 
that  orifice  (mitral  insufficiency,  mitral  regurgitation,  incompetency  of  the 
mitral  valve). 

Involvement  of  the  mitral  valve  alone  was  found  to  be  present  in  51  per  cent,  of  1781 
cases  of  valvular  disease  admitted  to  the  Johns  Hopkins  Hospital  between  1889  and  1908, 
and  in  54  per  cent,  of  Sperling's  300  autopsies  on  similar  cases  in  Virchow's  Pathological 
Institute  in  Berlin.  (Fig.  179.)  Mitral  insufficiency,  both  alone  and  in  association  with 
other  lesions,  was  present  in  64  per  cent,  of  the  Johns  Hopkins  cases,  occurring  alone  in 
29  per  cent,  (see  the  Table,  Fig.  179). 

As  regards  age,  Gillespie  (Fig.  178)  has  found  from  a  study  of  816 
cases  that  its  frequency  is  about  uniform  between  ten  and  fifty  years,  after 
which  it  diminishes.  This  is  in  sharp  contrast  to  the  cases  of  mitral  ste- 
nosis, which  are  most  frequent  before  the  age  of  thirty  and  become  much 
rarer  after  thirty.  In  youth  women  are  slightly  more  often  affected;  in  old 
age  the  affection  is  a  little  more  common  among  men.  The  mortality  from 
mitral  insufficiency  becomes  greater  as  age  progresses. 

PATHOLOGICAL    ANATOMY. 

Pathologically,  cases  of  mitral  insufficiency  may  be  divided  into  two 
groups : 

1.  Organic,  due  to  vegetations,  cicatrizations,  or  atheromatous  plaques, 
thickening  of  the  edges  of  the  valves,  or  ulceration  upon  the  valve  itself. 

2.  Functional  (or  relative),  in  which  the  valves  are  intact,  but  closure 
becomes  imperfect  through  relaxation  of  the  muscle  into  which  the  cusps 
are  inserted,  or  through  stretching  of  the  chordae  tendinese. 

Organic  Mitral  Insufficiency.  —  The  pathogenesis  of  organic  insuffi- 
ciency is  simple.  The  lesions  arise  during  the  course  of  an  acute  or 
subacute  endocarditis,  and  frequently  result  from  the  accumulation  of 
inflammatory  exudates  from  several  successive  infections.  These  are 
cemented  into  permanent  structures  by  organization  and  calcification. 
Occasionally  a  perforation  of  the  valve  occurs  from  ulceration.  As  in 
acute  endocarditis,  infection  in  the  rheumatic  cycle  is  the  most  common 
cause  of  chronic  mitral  disease,  though  other  infections  may  represent  not 
only  primary  but  exacerbating  factors. 

The  vegetation,  once  formed,  gives  rise  to  the  leak  by  holding  apart 
the  neighboring  portions  of  the  cusps  so  that  regurgitant  streams  occur 
about  its  serrations  (Fig.  180,  a.  A). 

21  321 


322 


DISEASES   OF   THE   HEART   AND   AORTA. 


Tests  for  Sufficiency  of  Mitral  Valve. — It  is  easy  to  demonstrate  by  the  method  of 
Gad  (see  page  10)  and  Meigs  that  when  the  vegetation  is  not  extensive  the  mitral  cusps 
may  adapt  themselves  perfectly  to  its  contour  and  prevent  a  leak  altogether;  but  when, 
as  is  usually  the  case,  their  flexibility  is  altered  by  a  line  of  vegetation,  atheroma,  or  infil- 
tration, this  apposition  is  prevented.  The  amount  of  blood  actually  regurgitating,  and 
hence  the  functional  importance  of  the  lesion,  depends  largely  upon  these  factors,  as  well 
as  upon  the  concomitant  affection  of  the  cardiac  muscle. 

At  the  autopsy  table  the  mitral  valves  may  be  tested  for  leakage  in  either  of  the 
following  ways: 

(1)  Water  may  be  forced  into  the  ventricle  through  a  cannula  attached  to  the  water 
faucet.     The  valve  usually  holds  against  leakage.     (T.  W.  King,  1837,  G.  A.  Gibson,  Meigs.) 

(2)  A  slit  is  made  in  the  ventricle  wall  near  the  apex.  The  heart  is  turned  upside 
down,  the  slit  at  the  apex  is  held  open  with  the  fingers  and  water  poured  in  from  above. 
The  normal  valve  would  show  no  leakage  (Bleichroeder). 


Fig.  180. — Regurgitant  streams  in  organic  and  functional  mitral  insuflSciencies.  A,  organic  mitral 
insuflSciency;  B,  functional  insufficiency  of  the  papillary  type;  C,  relative  mitral  insufficiency;  a,  view 
from  above  the  valves  ;  b,  coronary  section  through  the  heart.  The  arrows  indicate  the  points  and  direc- 
tion of  regurgitations. 

Coexistence  of  Organic  and  Functional  Insufficiency. — As  has  been 
stated  above  (page  226) ,  Koester,  Krehl,  Geipel,  and  others  have  shown  that 
the  occurrence  of  vegetations  upon  the  valves  is  often,  perhaps  usually, 
accompanied  by  foci  of  myocarditis  in  the  papillary  mus- 
cles and  in  the  ring  of  musculature  about  the  mitral  orifice.  It  is  the 
weakening  of  these  muscle-fibres  especially  which  gives  rise  to  the  func- 
tional insufficiencies,  and  it  is  therefore  probable  that  in 
many  cases  of  organic  mitral  insufficiency  the  ele- 
ment of  superadded  muscular  insufficiency  is  a  very 
important  one.  Indeed  one  often  meets  with  persons  who,  in  spite 
of  medium-sized  vegetations,  suffer  little  or  no  discomfort  as  long  as  the 
heart  muscle  is  in  good  condition,  but  in  whom  cardiac  symptoms 
occur  as  soon  as  overstrain,  anaemia,  or  febrile  disease  weakens  the  myo- 


MITRAL   INSUFFICIENCY.  .   323 

cardium.  In  the  periods  of  apparent  health,  the  leak  is  confined  to  the 
streams  about  the  edges  of  the  vegetation.  In  the  added  functional  insuf- 
ficiency it  also  takes  place  at  other  points  along  the  line  of  closure.  How- 
ever, it  is  impossible  to  differentiate  clinically  between  the  organic  and  the 
functional  elements,  and  their  relative  importance  in  a  given  case  cannot 
be  accurately  estimated. 

Atheroma  of  the  Mitral  Valve. — Atheromatous  and  calcified  patches  along  the  face 
and  edges  of  the  cusps  of  the  valves  are  also  not  uncommon  (see  Fig.  275,  page  469). 
These  changes  are  particularly  frequent  along  the  line  of  closure,  where,  as  shown  by  Roy 
and  Adami,  mechanical  injury,  hemorrhages,  and  exudates  are  most  frequent.  Patho- 
logically, they  are  brought  about  by  processes  similar  to  those  occurring  in  the  walls  of  the 
arteries  during  arteriosclerosis,  and  the  condition  is  frequently  associated  with  extensive 
sclerosis  of  the  coronary  arteries.  Calcified  plaques  may  also  be  present  in  the  myocardium 
(case  of  J.  L.,  Fig.  275).  The  mechanical  effect  of  such  thickenings  and  areas  of  rigidity 
is  to  prevent  the  cusps  from  accommodating  themselves  to  one  another,  giving  rise  to  leaks 
which  are  undistinguishable  clinically  from  those  due  to  vegetations. 

Hemorrhage  in  the  Mitral  Valve. — Occasionally  hemorrhages  occur  in  the  cusps  of 
the  mitral  valve,  especially  after  trauma  to  the  chest  (Kiilbs)  or  labor  (Weber  and 
Deguy),  and  in  new-born  infants  (Fahr).  It  is  probable  that  the  organization  of  the  clot 
initiates  a  fibrosis  which  leads  to  mitral  stenosis. 

Functional  Mitral  Insufficiency. — When  the  heart  muscle  attains  a 
certain  degree  of  weakness,  leaks  at  the  mitral  orifice  may  take  place. 
They  may  occur  as  the  direct  result  of  acute  cardiac  dilatation  from  a  pri- 
mary cardiac  overstrain,  though  they  arise  more  frequently  in  hearts  whose 
myocardium  has  already  undergone  degenerative  or  fibrous  changes  but 
whose  valves  are  still  intact.  This  functional  insufficiency  is  often  seen  in 
cases  of  myocarditis.  On  the  other  hand,  functional  insufficiency  of  the 
mitral  valve  may  arise  as  a  secondary  manifestation  in  organic  disease  of  the 
aortic  valves.  This  occurs  especially  when  the  leak  attains  a  severe  grade  or 
the  work  of  the  heart  is  too  much  increased,  the  walls  of  the  ventricle  and 
the  papillary  muscles  becoming  overstretched  during  diastole.  This  phe- 
nomenon will  be  further  discussed  in  the  chapter  upon  aortic  insufficiency. 

Types  of  Functional  Insufficiency. — The  leaks  occurring  at  the  mitral 
valve  as  the  result  of  muscular  weakness  may  be  divided  into  two  groups: 

1.  Papillary  Insufficiency. — Leaks  occurring  at  one  or  more  points  along  the 
valve  (Fig.  180,  B,  b)  when  the  weakness  of  a  papillary  muscle  or  stretching  of  a  chorda 
tendinea  allows  the  corresponding  portion  of  the  valve  to  be  lifted  a  httle,  and  a  small 
regurgitant  stream  to  emerge  at  one  of  the  points  of  pouting  and  puckering  along  the  line 
of  closure.  This  may  be  termed  the  type  of  papillary  insufficiency,  and 
like  many  cases  of  uncomplicated  organic  insufficiency  may  correspond  to  the  escape  of 
only  a  small  quantity  of  blood.  This  papillary  insufficiency  represents  the  mildest  form  of 
functional  regurgitation.  The  mitral  valve  is  pushed  upward  during  systole,  like  a  sail, 
impelled  by  the  full  force  of  the  entire  ventricular  wall.  This  is  antagonized  by  the  pull 
of  the  relatively  bmall  papillary  muscles.  It  is  evident  that  fibre  for  fibre  the  papillary 
muscles  incur  a  much  greater  strain  than  the  fibres  in  the  ventricular  wall,  and  consequently 
they  are  often  the  first  to  weaken.  When  they  weaken  api)osition  of  the  cusps  is  impaired 
and  regurgitation  sets  in.  Moreover,  since  T.  W.  King  and  Gibson  have  shown  that  the 
normal  mitral  valve  usually  holds  unless  dilatation  sets  in,  it  is  evident  that  the  papillary 
type  of  insufficiency  is  the  only  form  of  functional  insufficiency  that  can  occur  in  a  heart 
that  is  not  greatly  dilated. 

2.  Relative  Insufficiency. — The  second  type  of  functional  insufficiency  is  met  with 
when  the  left  ventricle  is  dilated  to  such  an  extent  that  the  mitral 
orifice  becomes  larger  than  the  available  area  of  valve  surface, 
and  what   may  be    correctly  termed   a    relative    insufficiency    results.      Under 


324 


DISEASES   OF   THE    HEART    AND    AORTA. 


these  conditions  the  leak  occurs  not  at  a  single  point  but  all  along  the  line  of  closure  (Fig. 
180,  C).  The  amount  of  blood  which  regurgitates  under  these  conditions  may  be  very  large. 
Pathogenesis  of  these  Types. — The  mode  of  occurrence  of  these  types  of  in- 
sufficiency may  be  readily  demonstrated  by  the  method  of  Gad  and  Meigs,  though  care 
must  be  taken  that  the  heart  used  for  the  experiment  is  not  in  a  condition  of  rigor  mortis. 
If  water  is  forced  into  the  ventricles  at  various  pressures,  it  will  be  seen  that,  as  shown  by  G. 
A.  Gibson,  leakage  will  occur  at  a  relatively  slight  pressure.  This  regurgitation  will  be 
small  in  amount,  and  will  be  seen  to  be  of  the  papillary  type;  but  if  the  pressure  is  suffi- 
ciently increased  and  the  ventricle  dilated,  the  cusps  of  the  valve  stand  apart,  the  true 
relative  insufficiency  (type  2)  is  produced,  and  a  large  amount  of  fluid  regurgitates.  The 
role  which  stretching  of  the  muscle  plays  in  this  regurgitation  may  be  shown  by  boiling  the 
heart  and  thereby  shortening  the  fibres  in  heat  rigor,  after  wliich  the  leak  that  was  present 
disappears  and  does  not  recur  until  much  greater  pressures  are  resorted  to.  Gibson  has 
caused  the  leak  to  disappear  by  tightening  a  ligature  about  the  mitral  muscular  ring.  It  is 
therefore  evident  that  the  tonicity  of  the  cardiac  muscle  is  an  important  element  in  deter- 
mining the  occurrence  and  the  degree  of  leak  both  in  functional  and  in  organic  mitral  insuffi- 
ciency. This  point  is  of  the  greatest  importance  in  therapeutic  considerations,  and  will  be 
referred  to  later. 

Occurrence  of  Functional  Insufficiency. — Functional  insufficiency  of 
the  mitral  valve  occurs  in  primary  cardiac  overstrain,  in  anamias,  during 
the  course  of  and  convalescence  from  infectious  diseases,  and  in  many 
cases  of  aortic  disease.  A  certain  percentage  of  the  cases  in  which  aortic 
and  mitral  insufficiencies  are  found  simultaneously  belongs  to  this  group. 

Lian,  in  Fran^ois-Franck's  laboratory,  has  shown  that  the  contraction 
of  the  ring  of  muscle  about  the  mitral  valve  (mitro-aortic  ring)  narrows 
the  diameter  of  the  orifice  during  systole.  He  demonstrated  that  when 
contraction  is  weakened  the  valves  may  not  remain  in  perfect  apposition. 

MECHANICS    OF    THE    CIRCUL.\TION    IX    MITRAL    INSUFFICIENCY, 

It  is  almost  axiomatic  to  state  that  the  systolic  regurgitation  of  blood 
from  left  ventricle  to  left  auricle  in  mitral  insufficiency  is  accompanied  by 
a  fall  of  pressure  in  the  former  and  a  rise  of  pressure  in  the  latter. 


^^^1     I 


COMPENSATED 


BROKEN  PULMONARY  COMPENSATION 


Fig.  181. — Diagram  showing  the  volume  and  pressure  curves  under  these  conditions.  (Schematic.) 
Upper  curve  (A),  interauricular  pressure;  solid  black  line,  volume  curve  of  the  left  auricle;  lower  curve 
(V),  intraventricular  pressure. 


The  regurgitation  of  blood  into  the  left  auricle  causes  a  systolic  rise  of 
pressure  to  take  place  in  this  chamber,  replacing  the  systolic  fall  of  pressure 
which  is  present  under  normal  conditions  (Fig.  181).  The  pressure  curve 
within  this  chamber  in  mitral  insufficiency  thus  resembles  that  seen  in  the 
right  auricle  in  tricuspid  insufficiency — a  rise  throughout  ventricular  systole 
with  a  fall  during  diastole,  and  a  small  rise  when  systole  of  the  auricle 
takes  place. 


MITRAL   INSUFFICIENCY.  325 

The  pressure  conditions  within  the  pulmonary  circulation  are  of  the 
greatest  importance,  and  in  this  both  the  force-pump  and  the  suction- 
pump  actions  of  the  ventricle  show  themselves. 

Effect  of  Mitral  Insufficiency  without  Increase  in  the  Strength  of  the 
Ventricle. — If  the  force  of  the  left  ventricle  remains  unaltered  after  the 
production  of  the  insufficiency,  it  stands  to  reason  that  less  blood  will  reach 
the  arteries  and  pass  on  to  the  capillaries  and  systemic  veins  than  did  so 
before.  The  arterial  blood-pressure  will  fall.  Consequently  less  blood  will 
enter  the  right  side  of  the  heart  from  the  venae  cavae,  and  the  pressure  in  the 
latter  will  be  lowered.  The  systolic  output  of  the  right  ventricle  will  thus 
be  diminished  and  the  pressure  in  the  pulmonary  artery  will  fall.  On  the 
other  hand,  the  regurgitated  blood  in  the  left  auricle  and  pulmonary  veins 
added  to  that  coming  on  from  the  pulmonary  artery  will  cause  the  pres- 
sure in  the  left  auricle,  the  pulmonary  veins,  and  the  capillaries  of  the  lungs 
to  rise  (Fig.  183,  III). 


Fig.  182. — Curve  of  intraventricular  pressure  in  mitral  insufficiency  produced  on  a  mechanical 
model.  (After  Marey.)  P.  V.,  intraventricular  pressure;  P.  R.,  arterial  pressure.  The  horizontal  line 
denotes  the  production  of  insufficiency.  O,  notch  due  to  the  auricular  systole;  e,  summit  of  the  curve 
during  systole  of  the  ventricle. 

Pulmonary  Stasis. — As  v.  Basch  and  his  pupils  have  shown,  conges- 
tion of  the  pulmonary  capillaries  is  the  most  important  cause  of  cardiac 
dyspnoea  (broken  pulmonary  compensation).  Hence  it  will  not  be  sur- 
prising that  dyspnoea  from  this  cause  is  an  early  and  important  symptom 
of  mitral  insufficiency,  and  that  its  disappearance  depends  upon  other 
factors  which  tend  to  deplete  the  pulmonary  capillaries.  (Diminution  in 
the  amount  of  blood  entering  right  ventricle,  or  weakened  suction-pump 
action  of  left.)  The  capillary  area  is  sufficiently  elastic  to  accommodate  a 
considerable  amount  of  regurgitant  blood  before  this  furnishes  an  obstruc- 
tion to  the  pulmonary  artery,  just  as  is  the  case  with  the  capillaries  of  the 
splanchnic  area,  but  after  a  time  or  in  severe  lesions  the  intrapulmonary  stasis 
finally  makes  its  effect  felt  in  the  pulmonar}^  artery.  The  pressure  there  rises 
(Gerhardt) .  When  the  pulmonary  stasis  becomes  extreme  the  right  ventricle, 
too,  becomes  overloaded  and  dilated.  Broken  systemic  compen- 
sation sets  in  (Fig.  183,  IV).  Stasis  occurs  in  the  systemic  veins, 
oedema  and  ascites  take  place,  and  a  secondary  functional  insufficiency  of 
the  tricuspid  valve  may  usually  be  demonstrated.  With  the  occurrence  of 
this  secondary  leak  at  the  tricuspid  orifice,  less  blood  is  pumped  into  the 
pulmonary  circulation,  the  congestion  here  diminishes,  the  dyspnoea  dimin- 


326 


DISEASES   OF   THE    HEART    AXD    AORTA. 


ishes  also,  and  in  spite  of  the  increased  gravity  of  the  condition  the  patient 
may  experience  some  temporary  relief  from  his  symptoms.  This  phenom- 
enon was  noted  by  T.  W.  King  in  1837,  and  was  designated  by  him  "the 
safety-valve  action  of  the  tricuspid  valve."  The  relief  is,  however,  only 
transitorj',  as  the  accumulation  of  COj  in  the  blood  soon  gives  rise  to 
dyspnoea  from  stimulation  of  the  respiratory  centre  in  the  medulla,  and  the 
real  state  of  cardiac  failure  manifests  itself.  If  the  condition  is  allowed  to 
continue,  the  outcome  is  death. 


Fig.  183. — Diagram  showing  the  effects  of  mitral  insufficiency  upon  the  circulation.  I.  Normal. 
II.  Compensation  through  filling  of  the  auricle  in  systole  but  complete  emptying  in  diastole.  III.  Broken 
pulmonary  compensation.     IV.  Broken  systemic  compensation. 

Effect  of  Increase  in  the  Strength  of  the  Left  Ventricle. — If,  on  the 

other  hand,  the  force  of  the  left  ventricle  increases,  it  can  throw  more 
blood  out  into  the  aorta  and  arteries;  and  this  blood  must  first  be  drawn 
from  the  left  auricle  and  pulmonary  circulation.  So  that  if  the  output 
from  the  ventricle  increase,  it  will  soon  be  pumping  more  blood  into 
the  aorta  than  the  right  ventricle  (whose  force  has  remained  practically 
unchanged)  pumps  into  the  pulmonary  SLTtery.  Accordingly  more  blood 
leaves  the  lungs  than  enters  them,  and  the  engorgement  passes  off.  The 
whole  condition  may  be  summed  up  by  the  statement  that  a  weakly 
acting  left  ventricle  overfills  the  lungs  with  blood, 
while  a  strongly  acting  left  ventricle  bails  them  out. 
The  whole  of  pulmonary  engorgement  is,  as  rightly 
claimed  by  v.  Basch,  a  problem  not  of  the  right  ventri- 
cle,  but   of  the   left. 


CLINICAL    MANIFESTATIONS. 
MITRAL   INSUFFICIEXCY    WITHOUT    SYMPTOMS. 

The  earliest  circulatory  disturbance  in  mitral  insufficiency  is  stasis  in 
the  pulmonary  capillaries,  which,  as  v.  Basch  and  his  pupils  have  shown, 
leads  to  cardiac  dyspnoea.  Accordingly,  it  is  not  surprising  that  dyspnoea 
should  be  one  of  the  earUest  symptoms  of  mitral  insufficiency.     But  the 


MITRAL   IXSUFFICIEXCY.  327 

pulmonary  stasis  does  not  occur  or  does  not  persist  when  the  action  of  the 
left  ventricle  is  sufficiently  vigorous,  and  hence  in  the  milder  cases  shortness 
of  breath  may  be  absent  for  a  long  time  after  the  actual  formation  of  the 
lesion  and  may  make  itself  evident  only  upon  exertion. 

Thus,  a  young  friend  of  the  writer,  a  boy  of  eleven,  in  1907  contracted  tonsillitis  accom- 
panied by  the  typical  signs  of  mitral  insufficiency.  He  was  kept  moderately  quiet  on  account 
of  the  throat  lesion  and  had  apparently  recovered  completely,  so  that  the  family  did  not 
notice  any  abnormality  until  a  year  afterward,  when  he  became  somewhat  short  of  breath 
upon  walking  uphill.  Since  a  little  caution  has  been  exercised  against  fast  walking  he  no 
longer  becomes  short  of  breath  and  remains  perfectly  free  from  symptoms.  The  prognosis 
is  very  favorable.  In  some  more  vigorous  individuals  the  lesion  does  not  manifest  itself 
at  all.  The  writer  has  in  mind  a  young  man  of  twenty-one  who  has  shown  signs  of  mitral 
insufficiency  for  eight  years,  but  during  that  period  has  excelled  at  football,  wrestling,  and 
all  the  severe  forms  of  sport;  also  a  professor  of  forty  who  has  had  a  mitral  lesion  of  rheumatic 
origin  for  some  time  without  the  slightest  physical  inconvenience.  These  cases,  though 
scarcely  to  be  regarded  as  the  rule,  are  encountered  with  great  frequency  in  patients  who 
are  examined  for  some  other  cause.  Occasionally  such  persons  have  been  informed  of  their 
trouble,  sometimes  given  a  grave  prognosis,  and  come  to  the  physician  in  great  mental 
distress  because  they  have  been  told  that  they  have  "organic  heart  trouble,"  and  yet 
they  may  reach  middle  or  even  old  age  without  serious  inconvenience.  It  is  not  extremely 
uncommon  to  find  cases  in  whom  a  mitral  lesion  has  been  present  thirty  or  forty  years  with- 
out greatly  affecting  the  patient's  activity  or  enjoyment  of  life. 

Pulmonary  Complications  of  Mitral  Disease.— The  prolonged  stasis  and  high  pres- 
sure in  the  pulmonary  capillaries  maj%  however,  give  rise  to  permanent  changes  in  their 
walls  and  in  the  tissues  about  them  and  facilitate  the  occurrence  of  a  chronic  bronchitis. 
This  bronchitis  resulting  from  stasis  may  be  considered  analogous  in  origin  to  the  ulcerations 
and  weeping  eczema  found  upon  the  legs  in  association  with  varicose  veins  or  cardiac  oedema. 
The  presence  of  this  chronic  bronchitis  is  Uable  to  arouse  a  suspicion  of  tubercu- 
losis when  the  trouble  is  really  cardiac.  The  suspicion  is  sometimes  still  further  aroused 
in  the  cases  in  which  the  walls  of  the  capillaries  in  some  area  of  the  lungs  have  become 
eroded  and  occasional  pulmonary  hemorrhages  take  place.  Thus,  Osier  and  A.  G.  Gibson 
mention  the  case  of  a  physician  who  suffered  from  occasional  haemoptysis  due  to 
mitral  insufficiency  over  a  period  of  twenty-five  years,  each  attack  giving  rise  to  great  relief 
of  his  cardiac  symptoms  by  relieving  the  engorgement  of  the  left  auricle.  The  diagnosis  in 
such  cases  is  often  difficult,  but  may  be  made  when  there  is  continued  absence  of  tubercle 
bacilli  from  the  sputum,  and  especially  from  the  ejected  blood,  associated  with  the  signs  of 
a  definite  mitral  insufficiency.  Further  confirmation  may  be  gained  by  a  negative  cuta- 
neous or  ophthalmic  reaction  with  tuberculin,  or  if  necessary  by  a  negative  subcutaneous 
injection  of  the  latter. 

MITRAL   INSUFFICIENCY    WITH    SYMPTOMS. 

Second  Stage  of  Mitral  Insufficiency  (Broken  Pulmonary  Compensa= 
tion). — A  more  severe  stage  with  less  favorable  prognosis  is  that  in  which  the 
lesion  manifests  itself  by  subjective  symptoms.  As  in  most  other  cardiac 
disturbances,  palpitation  occurs  early  in  the  disease.  Palpitation  is,  how- 
ever, common  in  healthy  persons,  and,  as  shown  by  Hirschfelder  (see  page 
157),  cannot  as  yet  be  regarded  as  signifying  functional  weakness,  so  that 
its  presence  scarcely  suffices  to  direct  suspicion  to  the  cardiac  valves. 

The  earliest  symptom  of  real  importance  is  shortness  of  breath. 
This  occurs  at  an  earlier  stage  in  affections  of  the  mitral  than  of  the  aortic 
valves,  but  is  more  marked  in  early  mitral  stenosis  than  in  early  mitral 
insufficiency.  Nevertheless,  it  may  be  quite  severe  in  compara- 
tively mild  grades  of  the  latter,  especially  on  exertion.  As  has 
been  stated  above,  the  dyspncBa  is  due  to  the  pulmonary  engorgement,  as 


328  DISEASES   OF   THE    HEART   AND    AORTA. 

shown  by  v.  Basch.  It  is  therefore  Uable  to  pass  off  when  the  left  ventricle 
hypertrophies  and  the  systolic  output  is  increased  and  the  suction-pump 
action  is  increased.  For  practical  purposes,  therefore,  such  persons  whose 
cardiac  function  has  been  restored  by  the  hypertrophy  of  the  left  ventricle 
may  be  said  to  have  passed  from  the  second  stage  insufficiency  back  into 
the  first.  They  often  remain  in  this  excellent  condition  for  a  number  of 
years,  and  sometimes  oscillate  between  the  first  and  the  second  stages  for 
a  number  of  years  more. 

Tonicity  of  the  Heart  as  a  Factor  Governing  the  Leak.  —  A  most 
important  factor  in  preserving  this  balance  is  the  tonicity  of  the  car- 
diac muscle;  for  when  the  tonus  is  maintained  the  cusps  of  the  valve 
are  approximated  as  tightly  as  possible  about  the  thickening,  and  the 
amount  of  leak  is  reduced  to  minimal,  whereas  when  the  tonicity  is  low 
the  organic  leak  is  further  supplemented  by  a  papillary  or  a  relative  insuf- 
ficiency. A  small  leak  is  thus,  if  only  for  a  time,  transformed 
into  a  large  one.  When  tonicity  is  low  it  is  harder  for  the  heart  to 
recover  from  such  an  additional  strain  than  if  the  latter  occur  at  a  time 
when  the  tonus  is  increased.  The  added  functional  insufficiency  may  thus 
become  permanent.    We  have  here  another  example  of  the  vicious  circle: 

Leak  at  mitral  valve 
Leak  increased  , 

Papillary  or     ^_     Heart  strain 
relative  insufficiency  Diminished  tonicity 

It  is  evident,  therefore,  that  in  spite  of  the  comparative  ease  with 
which  patients  may  recover  from  the  symptoms  of  mitral  insufficiency 
when  the  case  is  placed  under  favorable  conditions  as  soon  as  possible,  yet 
the  case  may  rapidly  become  a  grave  one  if  these  precautions  are  neglected, 
so  that,  in  the  words  of  Osier,  mitral  insufficiency  may  be  either  the  mildest 
or  the  gravest  of  valvular  lesions. 

Third  Stage  of  Mitral  Insufficiency  (Broken  Systemic  Compensa= 
tion). — The  second  stage  of  mitral  insufficiency  represents  the  physiological 
conditions  shown  in  Fig.  183,  IV,  when  the  stasis  is  in  the  lungs  and  the 
work  of  the  right  ventricle  is  gradually  increasing.  The  third  stage  repre- 
sents that  in  which  the  right  ventricle  also  has  begun  to  fail, 
and  blood  begins  to  stagnate  in  the  systemic  veins  as  well.  The  pressure 
in  these  veins  increases  two-  to  threefold  (from  5-8  cm.  HjO  to  20-30  cm.) 
as  can  be  shown  by  the  method  of  Eyster  and  Hooker.  As  a  result  they 
dilate  and  the  flow  through  them  is  slowed,  changes  occur  in  the  capillary 
walls,  and  oedema  soon  takes  place — first  in  the  feet,  later  in  the  shins, 
thighs,  genitalia,  and  back.  With  the  onset  of  these  manifestations  the 
shortness  of  breath  becomes  extreme,  a  dyspnoea  of  medullary  origin  adding 
its  effect  to  the  pulmonary  engorgement.  The  patient  is  compelled  to  sit  up 
all  the  time,  gasping  for  breath,  occasionally  with  paroxysms  of  real  cardiac 
asthma  and  palpitation,  sometimes  with  pains  in  the  heart,  severe  cough, 
and  expectoration  of  considerable  amounts  of  sputum  which  often  contains 
cells  loaded  with  blood  pigment  (Herzfehlerzellen) .  The  urine  becomes 
scant  and  loaded  with  albumin  and  casts.     Ascites  may  set  in  and  may 


MITRAL   IXSUFFICIEXCY. 


329 


even  become  so  great  as  to  require  repeated  tapping.  The  same  is  true  of 
hydrothorax.  On  this  account  it  is  more  common  upon  the  right  side. 
Unless  the  course  of  the  disease  is  checked,  death  may  follow  after  this 
stage  has  set  in ;  but  if  the  work  of  the  heart  can  be  diminished  and  its  action 
strengthened  it  may  soon  pump  out  the  stagnating  blood  and  lower  the 
venous  pressure.  From  this  cause,  and  owing  to  the  concomitant  increase 
in  cardiac  tonicity,  the  dilatation  diminishes.  The  element  of  regurgitation 
which  is  of  functional  origin  disappears  and  the  amount  of  blood  regurgi- 
tating is  once  more  reduced  to  that  which  flows  past  the  vegetations.  The 
work  of  the  heart  is  again  brought  to  its  minimum,  and  thus  it  is  that 
almost  unhoped-for  recoveries  may  occur  in  mitral  insufficiency 
when  properly  treated. 

PHYSICAL    EXAMINATION. 

Inspection. — The  typical  picture  of  mitral  disease  is  seen  in  the  flushed 
pink  cheeks  with  slight  tinge  of  purple,  slightly  dilated  venules,  and  bright 
watery  eyes,  giving  on  superficial  inspection  the  appearance  of  superabundant 
health — the  so-called  mitral  facies.  This  is  in  sharp  contrast  to  the  pale, 
pasty,  or  sallow  color  of  aortic  insufficiency,  or  the  livid  purple  of  emphysema. 
The  lips  show  a  moderate  cyanosis.  There  is,  as  a  rule,  no  special  throbbing 
seen  in  the  carotids.  The  venous  pulse  is  usually  well  seen  and  is  of  the 
normal  "double"  type.  Since 
the  disturbance  of  function  in 
the  first  two  stages  is  in  the  pul- 
monary circulation  and  not  in 
the  systemic,  no  change  in  the 
jugular  pulsation  is  to  be  found 
nor  would  be  expected  until  the 
third  stage,  when  the  onset  of 
tricuspid  insufficiency  causes  it 
to  assume  the  "single"  or  ven- 
tricular form. 

The  chest  may  show  pre- 
c  or  dial  bulging,  especially  in 
children  and  in  cases  of  long 
standing.  The  apex  impulse  if 
visible  is  displaced  out- 
wards toward  the  axilla 
rather  than  downwards. 
It  is  frequently  of  a  slow  heav- 
ing character,  while  in  cases  of 

long-standing  pulmonary  stasis  there  may  be  also  a  wavy  systolic  retrac- 
tion of  the  interspaces  which  mark  the  hypertrophy  of  the  right  ventricle. 
Occasionally  a  systoHc  impulse  in  the  second  left  interspace  shows  the 
vigorous  pulsation  of  the  pulmonary  artery.  In  very  large  hearts  it  is  not 
uncommon  to  find  a  systoHc  retraction  present  along  the  outer  border  of 
dulness,  even  when  adherent  pericardium  is  absent. 

In   long-standing    cases  changes  in  the  extremities  also  take  place, 
especially  slight  clubbing  of  the  fingers. 


Fig.  184. — Distribution  of  the  murmur  in  mitral  in- 
sufficiency. Distribution  upon  the  chest  wall.  Light 
line,  outline  of  cardiac  dulness;  heavy  line,  outline  of 
cardiac  flatness.  Shaded  area  shows  distribution  of  the 
murmur.  The  diagram  at  the  right  indicates  the  relation 
of  the  murmur  to  the  cardiac  cycle. 


330 


DISEASES   OF   THE    HEART    AND    AORTA. 


Fig.  185. — Cross  section  of  the  body  show- 
ing how  the  thrill  and  murmur  reach  the  chest 
wall.  The  heavily  stippled  areas  indicate  the  areas 
over  which  the  murmur  i.s  heard. 


Palpation  usually  reveals  a  strong,  slow,  heaving  impulse  with  a  more 
or  less  intense  thrill  lasting  throughout  the  period  of  systole.  This  thrill 
is  probably  due  to  the  impact  of  eddy  currents  passing  by  the  vegetation 
and  striking  the  heart  wall,  whose  impact  sets  the  valve  into  vibrations 
that  are  communicated  along  the  chordse  tendinese  to  the  walls  of  the 

heart  and  then  to  the  chest.  It  is  most 
intense  at  the  apex,  but  is  often  pal- 
pable over  the  entire  precordium,  oc- 
casionally in  the  axilla,  and  sometimes 
at  the  back  in  the  left  interscapular 
region.  The  thrill  at  the  back  is  rarely 
felt  except  in  children  and  thin- 
chested  persons,  but  as  it  represents 
the  direct  impact  of  regurgitation 
it  is  very  characteristic.  In  a  few 
cases  the  thrill  from  a  mitral  lesion 
can  be  felt  in  the  vessels  of  the 
neck,  and  sometimes  also  over  the 
entire  chest. 

The  shock  accompanying  the  second  heart  sound  is  practically  un- 
changed, though  it  is  often  more  distinct,  especially  over  the  pulmonary  area. 
Percussion. — The  characteristic  cardiac  outline  in  mitral  insufficiency 
shows  an  increase  in  area  horizontally  (M  L)  towards  the  left,  which  is  some- 
times enormous  and  may  reach  well  into  the  axilla  and  as  much  as  22  cm. 
from  the  midline  by  percussion.  When  the  apex  approaches  the  axillary 
convexity,  as  shown  by  Moritz, 
the  area  of  dulness  usually 
extends  somewhat  beyond  the 
actual  outline  of  the  heart;  but 
with  the  lightest  possible  percus 
sion  (the  threshold  percussion) 
this  error  may  often  be  reduced  to 
a  centimetre  or  less.  In  contrast 
to  the  cardiac  outline  in  aortic 
insufficiency,  the  left  border 
of  dulness  or  of  the 
shadow  seen  with  the 
X-ray  is  increased  diag- 
onally upwards  and  out- 
wards, as  well  as  outwards  in 
the  horizontal  diameter  (Fig. 
186).      The    upward    extension 

may  reach  the  second  rib  and  pass  outward  into  the  second  left  inter- 
space. According  to  the  autopsy  findings  of  Harris,  this  is  not  due  to  the 
dilatation  of  the  left  auricle,  but  to  the  increase  in  size  of  the  conus  arte- 
riosus of  the  right  ventricle  and  to  some  dilatation  of  the  pulmonary  artery. 

Harris  has  shown  that  even  an  extremely  dilated  left  auricle  is  not  visible  from 
the  front  of  the  chest  under  these  circumstances.  As  is  therefore  to  be  expected,  such  dila- 
tions correspond  to  the  later  rather  than  to  the  earlier  stages  of  the  disease,  and  are  also 


Fig.  186. — Radiograph  of  a  patient  with  mitral  in- 
sufficiency, showing  horizontal  enlargement  of  the  heart 
to  the  left.      (After  Bougsch  and  Schittenhelm.) 


MITRAL   INSUFFICIENCY. 


331 


more  common  in  mitral  stenosis  than  insufficiency.    The  cardiac  dulness  is  not  increased 
to  the  right  until  the  third  stage  of  the  disease. 

The  Systolic  Murmur. — The  data  obtained  from  auscultation  usually 
furnish  the  basis  for  the  diagnosis  of  mitral  insufficiency.  The  character- 
istic sign  is  the  presence  of  a  murmur  heard  at  the  apex  and  in  the 
left  axilla  throughout  systole, — i.e.,  last- 
ing up  to  the  second  sound.  The  sounds 
of  different  systolic  murmurs  are  described 
by  the  French  writers  as  resembling  the 
rasping  of  a  file,  the  sawing  of  wood,  the 
hissing  of  a  jet  of  steam,  the  cooing  of  a 
dove !  These  variations  depend  upon  many 
sound-producing  factors  so  complex  that  it 
is  impossible  to  predict  the  characteristics 
of  the  lesion  upon  the  valve  by  the  murmur 
to  which  it  gives  rise.  In  general,  rough, 
roaring,  sawing,  and  purring  murmurs  are 
very  often  produced  by  thickened  or  calcified 
vegetations,  which  act  more  or  less  as  sound- 
ing-boards, while  whispering  or  blowing  mur- 
murs are  produced  by  regurgitant  streams 
passing  over  smooth-walled  valves,  and 
occur  especially  in  functional  insufficiencies. 
However,  exceptions  to  this  are  frequent. 

Digital  Imitation  of  the  Mitral  Systolic  JVlurmur. — The  mitral  systolic  murmur  can  be 
reproduced  by  Larned's  or  Smith's  methods  by  a  stroke  across  the  elbow  or  across  the 
back  of  the  hand.  To  imitate  a  murmur  accompanying  the  first  sound  the  latter  should 
be  produced  by  a  slow  flexion  of  the  finger,  which  combines  the  blow  and  the  strok- 
ing. For  demonstrations  to  a  group  of  students  these  manoeuvres  may  be  carried  out 
upon  a  derby  hat.  The  stroke  should  be  of  long  duration  and  should  be  followed 
immediately  by  the  tap  which  represents  the  second  sound. 

Excellent  phonographic  tracings  of 
this  murmur  have  been  made  by  Eint- 
hoven  as  well  as  by  Weiss  and  Joachim. 
These  observers  have  shown  that  in  con- 
trast to  the  murmur  of  aortic  stenosis  the 
murmur  of  mitral  insufficiency  always 
begins  synchronously  with  the  first  sound. 
It  is  loudest  at  the  time  of  the 
first  sound,  which  it  may  entirely  re- 
place and  may  then  be  uniform  through- 
out the  period  of  systole  or  take 
on  a  decrescendo  character,  in 
murmur  which  folio  ws  the  first 
character. 


Fig.  187.  —  Diagram  of  Fig.  186. 
showing  the  directions  in  which  car- 
diac enlargement  has  taken  place.  The 
broken  line  represents  the  outline  of  the 
normal  heart.  The  arrows  indicate  the 
conjugates  (ML  and  L)  which  are  most 
enlarged. 


MUKMIR 


-1   , ;  (2. 


Fig.  188. — Graphic  records  of  the  heart 
sounds,  showing  the  systolic  murmur. 
(Kindness  of  Prof.  Einthoven.)  1,  2,  heart 
sounds.  The  vibrations  between  1  and  2 
and  some  of  those  composing  1  are  due  to 
the  murmur. 


in 


contrast    to    the    aortic 
sound  and  is  crescendo 

They  have  shown  further  that  in  some  cases  the  first  sound  and  murmur  precede 
the  carotid  wave  by  a  greater  interval  than  normally  (lengthening  of  the  presphygmic 
period  from  .08-.09  sec.  to  .12-.  15  sec).  At  the  very  beginning  of  systole  blood  rushes 
back  into  the  auricle.  This  escape  causes  the  pressure  in  the  ventricle  to  rise  more  slowly 
than  usual  and  hence  aortic  valves  open  a  little  later.     Hence  the  presphygmic  period  is 


332  DISEASES   OF   THE   HEART   AND    AORTA. 

later.  It  is  possible  that  the  duration  of  the  presphygmic  period  may  serve  as  a  guide 
to  indicate  the  degree  of  leakage, — shortening  indicating  an  improvement,  lengthening 
an  increase  in  leakage.  However,  other  observers  find  lengthened  presphygmic  periods 
from  different  causes. 

In  the  accidental  murmurs  of  anaemia  Weiss  and  Joachim  have  found  a  normal 
presphygmic  period. 

It  is  stated  by  some  writers  that  functional  murmurs  occur  late  in  systole,  mesosystolic 
or  telesystolic,  because  comparatively  little  regurgitation  occurs  until  the  intraventricular 
pressure  has  reached  its  maximum  and  the  papillary  muscles  begin  to  weaken.  There  are 
no  graphic  records  supporting  this  claim,  and  the  subject  demands  experimental  investiga- 
tion rather  than  clinical  speculation. 

As  regards  distribution,  the  murmur  of  mitral  insufficiency  is  heard 
over  those  areas  of  chest  wall  which  are  nearest  to  the  left  ventricle  and 
left  auricle,  namely,  the  apex  and  the  neighboring  areas  to  the  left  (Fig.  184). 

The  reason  why  the  murmur  of  mitral  insufficiency  is  heard  so  loudly  at  the  apex  is 
not  perfectly  clear,  since  this  propagation  is  opposite  to  the  direction  of  the  regurgitant 
stream.  It  is  possible,  however,  that  the  vibrations  of  the  mitral  valve  may  be  transmitted 
to  the  anterior  papillary  muscle  and  apex  by  the  papillary  muscles  which  act  like  vioUn 
strings.  This  would  also  explain  why  the  murmur  is  so  loud  in  the  anterior  part  of  the  left 
axilla  at  a  considerable  distance  from  the  left  auricle  but  near  the  anterior  papillarj'  muscle 
(Fig.  185). 

In  children  and  in  many  persons  with  small,  thin-walled  chests  the 
murmur  is  also  heard  over  the  left  interscapular  region  to  which  it  is  trans- 
mitted directly  from  the  left  auricle.  This  distribution  is  the  one  which  is 
most  typical,  since  it  represents  transmission  in  the  direction  of  leakage, 
and  the  comparative  infrequency  with  which  it  is  heard  is  due  entirely  to 
the  thickness  of  the  chest  wall  and  the  layer  of  lung.  Certain  excellent 
German  observers,,  however,  are  unwilling  to  diagnose  mitral  insufficiency 
unless  this  murmur  is  present. 

In  order  to  obviate  these  disturbing  factors,  August  Hoffmann  and  later  Gerhartz 
have  attempted  to  use  the  oesophageal  auscultation  described  on  page  1 04, 
but  it  is  unpleasant  to  the  patient,  and,  besides,  the  murmur  may  be  no  more  distinct 
than  at  the  apex. 

Another  rarer  site  for  the  systolic  murmur  of  mitral  insufficiency,  as  shown  by  Naunyn. 
is  the  pulmonary  area — the  second  and  third  left  interspaces  at  the  sternal  margin  and 
as  far  out  as  the  parasternal  line.  Naunyn  thinks  that  in  this  region  the  \ibrations  are 
communicated  by  the  hypertrophied  and  dilated  left  auricle  to  the  pulmonary  artery.  This 
murmur  must  always  be  carefully  differentiated  from  the  accidental  pulmonary  murmur 
heard  in  this  region  and  from  that  due  to  pulmonary  stenosis  and  sclerosis. 

Over  the  right  ventricle,  that  is  from  the  left  parasternal  line  to  the 
left  sternal  margin,  the  murmur  of  mitral  insufficiency  is  usually  heard, 
diminishing  in  intensity  as  the  distance  from  the  apex  increases. 

Differentiation  from  Accidental  and  Tricuspid  Murmurs. — This  is  in 
sharp  contrast  to  the  accidental  or  "haemic"  murmurs  which  are 
loudest  over  the  right  ventricle  and  especially  over  its  upper  portion  (in  the 
second  and  third  left  interspaces) .  These  murmurs  diminish  over  the  apex 
while  the  mitral  murmur  increases.  They  are  rarely  heard  to  the  left  of  the 
apex.  They  are  later,  softer,  shorter,  more  superficial;  they  vary  with 
inspiration,  expiration,  and  change  of  position;  and  the  heart  is,  as  a  rule, 
not  hypertrophied.  On  the  other  hand,  there  is  no  reason  to  believe  that 
the  distribution  of  the  murmur  due  to  functional  mitral  insufficiency  differs 
from  that  due  to  vegetations  upon  the  valves,  and  it  is  frequently  impos- 


MITRAL   INSUFFICIENCY.  333 

sible  to  diflFerentiate  between  the  two  conditions.'  The  common  statement 
that  murmurs  of  organic  origin  are  transmitted  to  the  axilla  while  those  of 
functional  origin  are  not  is  due  to  a  confusion  of  "functional"  with  "acci- 
dental" murmurs.  All  loud  and  rough  murmurs  are  transmitted  further 
than  soft  ones,  and  murmurs  due  to  vegetations  are  usually  louder  than 
functional  murmurs,  but  a  soft  murmur  of  organic  origin  is  probably  no 
louder  than  many  murmurs  of  functional  origin. 

The  murmur  due  to  tricuspid  insufficiency  is  heard  loudest  over  the 
lower  portion  of  the  sternum,  the  epigastrium,  and  often  also  to  the  right 
of  the  sternum.  That  of  aortic  sclerosis  or  aortic  stenosis  is  loudest  over 
the  second  and  first  right  interspace,  and  is  usually  transmitted  to  the 
carotid  and  axillary  arteries.  The  same  applies  to  the  murmur  due  to 
aneurism.  Moreover,  as  stated  by  Boy-Teissier,  it  is  always  meso-  or 
telcsystolic,  and  therefore  follows  but  never  replaces  the  first  sound. 

The  Second  "Sound. — The  second  sound  at  the  apex  and  over  the  aortic 
area  shows  no  special  change,  but  over  the  pulmonic  area  it  may  be  greatly 
accentuated.  This  is  not  always  the  case,  because,  as  seen  in  Fig.  183,  the 
pressure  in  the  pulmonary  artery  is  not  always  increased;  but  during  the 
course  of  a  mitral  insufficiency  the  intensity  of  the  second  pulmonic  may 
change.  In  interpreting  the  significance  of  this  change  it  must  be  remem- 
bered that  rise  of  pulmonary  pressure  may  occur  either  when  the  force  of 
both  ventricles  is  increasing  or  when  extreme  engorgement  of  the  pulmo- 
nary vessels  has  occurred.  In  the  former  case  it  will  be  accompanied  by  the 
general  signs  of  improvement  in  the  left  ventricle,  larger  pulse,  increased 
maximal  blood-pressure,  increased  pulse-pressure;  in  the  latter  case  by  fail- 
ure of  the  left  ventricle.  Regarding  the  role  which  vasomotor  changes  in 
the  pulmonary  vessels  play  under  clinical  conditions  little  is  known;  but 
they  also  can  affect  the  intensity  of  the  second  pulmonic. 

Pulse.  —  The  pulse  in  mitral  insufficiency  shows  no  characteristic 
changes.  Dependent  upon  blood-pressure,  systolic  output,  and  pulse-pres- 
sure which  vary  considerably,  it  may  be  large  or  small,  hard  or  soft.  De- 
pendent upon  the  condition  of  the  heart  muscle  and  especially  of  the  left 
auricle,  it  may  be  regular  or  irregular.  The  condition  of  the  individual 
patient  at  any  single  stage  of  the  disease  must  be  viewed  in  the  light  of 
these  determining  factors. 

BIood=pressure. — As  has  been  seen  above,  the  sudden  production  of 
mitral  insufficiency  both  in  animals  and  on  the  model  is  followed  directly  by 
a  fall  of  blood-pressure  and  diminution  of  pulse-pressure,  unless  the  strength 
of  the  ventricle  and  its  systolic  output  be  increased.  Such  an  increase  does 
take  place,  however,  during  hypertrophy,  and  hypertrophy  of  the  left 
ventricle  is  the  rule  in  mitral  insufficiency.  Moreover,  when  the  output 
into  the  arteries  is  diminished  by  the  backflow  into  the  left  auricle,  these 
vessels  undergo  a  compensatory  constriction  and  narrow  the  blood  channel. 
However,  as  the  left  ventricle  hypertrophies,  its  systolic  output  increases 
at  the  expense  of  the  residual  blood.  These  two  compensatory  factors 
combine  to  maintain  the  blood-pressure  and  pulse-pressure  at  their  original 

*  The  confusion  of  the  terms  "  hsemic  "  (accidental)  and  "  functional "  murmurs  so 
common  in  clinical  notes  seems  therefore  to  be  both  unnecessary  and  misleading,  and  should 
be  carefully  avoided. 


334  DISEASES   OF   THE   HEART    AND    AORTA. 

level,  and  at  times  even  exceed  it.  For  example,  a  prominent  medical 
educator  who  has  a  mild  leak  at  the  mitral  valve  but  suffers  no  symptoms, 
has  a  maximal  pressure  of  140,  a  minimal  of  95,  and  a  large  full  pulse.  The 
compensation  in  this  case  has  more  than  balanced  the  disturbance  in  the 
circulation.  This  increase  of  pulse-  and  blood-pressure  is  not  always  indica- 
tive of  improvement,  but  may  occur  also  as  terminal  events  under  the 
stimulation  of  medullary  asphyxia  (see  page  27),  On  the  other  hand,  the 
presence  of  a  rather  small  pulse  and  rather  low  blood-pressure  and  pulse- 
pressure  may  merely  represent  the  natural  effect  of  the  lesion  unaltered  by 
compensatory  changes  on  the  one  hand,  or  on  the  other  may  represent  the 
failure  of  the  left  ventricle  to  maintain  the  circulation.  The  presence  of 
arteriosclerosis  may  in  itself  tend  to  modify  the  blood-pressure,  and  to 
increase  a  blood-pressure  and  pulse-pressure  that  would  otherwise  be  small. 
In  any  case  the  blood-pressure  shows  no  characteristic  features  in  mitral 
insufficiency,  and  the  figures  obtained  are  to  be  viewed  as  the  algebraic 
sum  of  various  circulatory  factors,  rather  than  as  absolute  measures  of 
cardiac  vigor.  It  must  be  remembered  further  that  the  cardiac  symptoms 
are  due  mainly  to  changes  in  the  pulmonary  circulation,  while  the  blood- 
pressure  changes  are  concerned  only  with  the  systemic. 

Arrhythmia. — The  action  of  the  heart  is  often  irregular  in  mitral  dis- 
ease, so  that  the  arrhythmia  in  these  conditions  is  frequently  described  as 
"the  mitralized  pulse."  Physiologically,  the  "mitralized  pulse" 
represents  an  irregularity  probably  due  to  numerous  extrasystoles  arising 
in  the  left  auricle  but  so  frequent  as  to  disturb  the  rhythm  completely. 
In  contrast  to  the  absolute  irregularity  arising  in  the  right  auricle,  the  a 
wave  upon  the  jugular  tracing  may  persist  in  spite  of  the  arrhythmia,  for 
the  right  auricle  may  not  be  paralyzed.  Joachim  has  shown  by  oesophageal 
tracings  that  the  left  auricle  is  often  paralyzed  under  such  circumstances. 
With  the  irregularity  there  are  often  very  feeble  early  extrasystoles  too 
weak  to  open  the  aortic  valves  and  to  cause  a  pulse  wave.  The  second 
heart  sound  is  lacking  with  these  beats  because  the  valves  are  not  opened. 

The  origin  of  the  irregularity  is  probably  in  the  distended  left  auricle 
(cf.  also  page  75).  It  is  sometimes,  but  by  no  means  always,  accompanied 
by  paralysis  of  the  auricle,  as  shown  by  the  venous  tracings,  but  the  exact 
mechanism  by  which  this  form  of  irregularity  is  produced  requires  further 
investigation  in  order  that  its  diagnostic  and  prognostic  significance  may 
be  thoroughly  understood. 

The  condition  of  the  radial,  temporal,  and  other  arteries  may  vary 
considerably,  but,  especially  in  patients  above  40,  may  show  considerable 
grades  of  arteriosclerosis.  This  is  more  common  and  somewhat  m.ore  exten- 
sive in  patients  suffering  from  any  cardiac  disease  than  in  persons  with 
normal  hearts  (Wild). 

Lungs. — Examination  of  the  thorax  and  lungs  in  mitral  insufficiency 
reveals  the  usual  signs  corresponding  to  the  pulmonary  changes  described 
above — small,  moist,  and  piping  rales  corresponding  to  the  bronchitis  often 
associated  with  hyper-resonance  on  percussion.  Over  areas  of  hydrothorax 
there  are  absolute  flatness  on  percussion,  absence  of  vocal  fremitus  and 
breath  sounds,  Koranyi's  flatness  over  the  lower  thoracic  spines,  and 
Grocco's  triangle,  paravertebral  dulness  to  the  left  of  the  midline. 


MITRAL   INSUFFICIENCY.  335 

Abdomen. — The  abdomen  rarely  shows  any  special  change  during  the 
milder  stages  of  the  disease.  Occasionally  one  finds,  as  in  a  young  girl 
recently  under  the  writer's  observation  in  the  Johns  Hopkins  Dispensary, 
the  remains  of  an  old  splenic  infarction,  characterized  by  enlargement, 
hardness,  and  tenderness  of  the  organ.  This  may  persist  for  some  months. 
Enlargement  and  pulsation  of  the  liver  and  ascites  (portal  stasis)  belong  to 
the  stage  of  broken  systemic  compensation  (see  page  338) .  The  same  also 
applies  to  oedema  of  the  feet,  ankles,  and  legs,  which  occurs  in  the  mildest 
form  of  broken  compensation.  These  phenomena,  though  of  serious  import, 
are  by  no  means  harbingers  of  death,  for  with  proper  treatment  many  cases 
outlive  one  or  even  several  breaks  in  compensation  for  many  years. 

The  following  represent  the  course  of  typical  cases  of  mitral  insuf- 
ficiency. 

Case  of  Mitral  Insufficiency. 

C.  H.,  ship  carpenter,  aged  63,  first  admitted  to  the  Johns  Hopkins  Hospital  jn  No- 
vember, 1899,  complaining  of  shortness  of  breath.  Family  history  negative.  The 
patient  has  always  been  a  robust  man.  He  gives  a  doubtful  history  of  rheumatism, 
but  a  definite  history  of  pneumonia  five  years  before  admission.  No  venereal  his- 
tory.    He  has  always  been  a  hard  eater,  hard  drinker,  and  a  hard  worker. 

The  present  illness  began  with  attacks  of  paroxysmal  dyspnoea  upon 
exertion  eight  or  nine  months  before  admission.  Two  months  before  admission  an 
attack  came  on  spontaneously  while  in  a  warm  room.  During  the  past  month  he  has 
not  been  able  to  lie  down  in  bed  owing  to  dyspnoea  and  the  onset  of 
a  smothering  feeling.  He  has  had  no  cough,  no  haemoptysis.  Examination  on  this  admis- 
sion showed  a  stout,  well-nourished  man  with  mucous  membranes  a  trifle  purple  and  dilated 
venules  over  the  face.  His  chest  was  barrel  shaped  and  there  was  a  little  fluid  (flatness  and 
impaired  breath  sounds)  at  the  bases  behind. 

Heart. — Apex  was  situated  in  the  6th  interspace  16.5  cm.  from  the  midline.  The 
area  of  cardiac  dulness  reached  upward  to  the  second  costal  cartilage  and  5  cm.  to  the 
right  of  the  sternum.  There  is  a  well-marked  systolic  murmur  heard  over  the 
body  of  the  heart  and  over  the  anterior  part  of  the  axilla.  The  second  sound  is  every- 
where clear;  the  second  aortic  booming. 

The  hver  is  slightly  enlarged,  being  just  palpable;  the  spleen  is  not.  The  abdomen  is 
full,  the  flanks  bulge,  and  there  is  slight  movable  dulness  in  the  flanks.  Genitalia  normal. 
There  is  slight  oedema  of  the  ankles.  Blood  count  normal.  Urine  is  dark  sherry 
colored,  specific  giavity  1024,  acid,  contains  a  small  amount  of  albumin  and  some  hyaUne 
and  granular  casts. 

The  patient  was  put  to  bed  on  soft  diet,  given  daily  purgation  with 
magnesium  sulphate  (30  Gm.,  oi),  also  8  doses  of  tincture  of  digitalis  (1  c.c,  tt\^xv) 
at  intervals  of  four  hours,  followed  up  by  strychnine  1.5  mg.  He  was  also  given 
potassium  iodide  1  Gm.  (gr.  xv)  after  meals. 

QMema  disappeared  and  orthopncea  also,  so  that  within  ten  days  the  patient  could 
sleep  with  his  head  low  and  could  walk  without  dyspnoea.    He  then  left  the  hospital. 

He  was  next  seen  three  years  later,  having  been  perfectly  well  until 
he  took  cold  one  month  before,  since  when  he  had  shortness  of  breath  on  exertion  and 
on  lying  down.  He  had  some  cough  and  slight  swelling  of  the  feet.  The  physical 
condition  was  about  as  on  the  first  admission,  except  that  the  systolic  murmur 
entirely  replaced  the  first  sound  and  was  well  heard  in  the  axilla. 
Maximal  blood-pressure  182  mm.  Hg.  He  again  improved  rapidly  and  left  the  hospital 
in  two  weeks. 

He  entered  the  hospital  again  one  year  later  with  the  same  signs,  the  liver  being  now 
2  cm.  below  the  costal  margin.  Once  more  he  improved  rapidly  under  treatment;  the  liver 
receded,  and  he  was  discharged,  only  to  be  readmitted  in  the  same  condition  five  weeks  later, 
when  symptoms  dated  from  exposure  to  the  wet.  He  then  had  some  tenacious  sputum 
streaked  with  blood  and  numerous  moist  rales  were  heard  everywhere  over  his  chest.  Re- 
covery was  once  more  imeventful. 


336  DISEASES   OF   THE    HEART    AND    AORTA. 


COMPLICATIONS    AND    SEQUELS. 

There  are  few  complications  and  sequelae  which  are  more  character- 
istic of  mitral  insufficiency  than  of  other  valvular  diseases.  Those  symp- 
toms due  to  pulmonary  engorgement,  bronchitis,  haemoptysis,  and 
pulmonary  oedema  have  already  been  discussed.  Embolism  from  loosening 
of  vegetations  upon  the  mitral  valve  or  of  clots  which  have  formed  in  the 
left  auricle  during  periods  of  stasis  is  an  occasional  occurrence,  especially 
in  severe  cases,  but  less  common  than  in  mitral  stenosis.  As  the  result 
of  this  there  may  be  the  production  of  infarcts  in  the  various  organs — 
spleen,  kidneys,  and  brain — and  of  ecchymoses  in  the  skin. 

In  contrast  to  mitral  stenosis,  pulmonary  tuberculosis  occurs  in  mitral 
insufficiency  with  the  same  frequency  as  in  otherwise  normal  individuals 
(Meisenburg) . 

As  may  be  seen  in  Fig.  166,  mitral  insufficiency  is  very  frequently  asso- 
ciated with  other  valvular  diseases,  29  per  cent,  of  all  the  cases  of  valvular 
disease  at  the  Johns  Hopkins  Hospital  being  accompanied  by  aortic  insuffi- 
ciency, 21  per  cent,  by  mitral  stenosis.  In  these  cases  the  mitral  insuffi- 
ciency is  sometimes  the  original  lesion,  the  other  lesion  resulting  from  a 
metastatic  infection  or  subsequent  organization.  On  the  other  hand,  the 
mitral  insufficiency  associated  with  aortic  insufficiency  may  also  be  a  func- 
tional one  due  to  overfilling  of  the  ventricles.  The  mitral  insufficiency 
which  appears  late  in  the  course  of  mitral  stenosis  is  due  to  the  inability  of 
the  thickened  valves  to  close.  Coronary  sclerosis,  as  shown  by  Wild,  is 
more  than  usually  common  in  chronic  valvular  disease,  and  hence  should 
be  borne  in  mind  in  establishing  the  prognosis. 

Pericarditis  is  one  of  the  common  complications,  especially  in  children, 
in  whom  adhesive  pericarditis  is  to  be  feared. 

Since  the  majority  of  cases  of  mitral  disease  are  of  rheumatic  origin, 
diseases  of  the  rheumatic  cycle,  tonsillitis,  articular  rheumatism,  chorea 
in  children,  and  affections  of  the  urticarial  group,  are  particularly  common. 
Of  these  arthritis  is  the  most  frequent  as  well  as  the  most  stubborn 
and  dangerous. 

TREATMENT. 

The  management  of  cases  of  mitral  disease  does  not  depart  in  any 
essential  particular  from  the  general  type  of  treatment  of  cardiac  disease. 
It  should  be  directed  to  three  ends: 

1.  Removing  the  overstrain; 

2.  Increasing  the  strength  of  the  heart; 

3.  Avoidance  of  infection,  and  removal  of  the  foci. 

In  the  mildest  cases,  the  insufficiency  shown  by  signs  but  not  by  symp- 
toms, due  especially  to  the  formation  of  a  new  vegetation,  it  is  most  impor- 
tant that  the  cardiac  tonicity  should  be  maintained,  that  the  amount  of 
leakage  should  thus  be  kept  down  to  its  minimum,  and  that  cardiac  hyper- 
trophy should  be  induced  before  symptoms  have  set  in.  It  is  therefore 
most  important  to  spare  the  heart  every  effort.  If  the  patient  is  seen  at 
the  onset  of  the  disease  he  should  be  kept  at  absolute  rest  in  bed  for  at 
least  a  couple  of  weeks  after  temperature  has  returned  to  normal  and  all 


MITRAL   INSUFFICIENCY.  337 

signs  of  acute  disease  have  passed.  Too  much  care  cannot  be  exercised 
at  this  time,  since  this  is  the  crucial  epoch  in  determining  the  severity  of 
the  case.  It  is  important  not  only  to  maintain  the  tonicity  of  the  heart 
muscle  but  to  preserve  the  valves  from  all  further  injuiy  until  the  vegeta- 
tions have  become  thoroughly  organized  and  lined  with  endothelium,  and 
the  germs  have  disappeared  from  the  original  focus  of  infection.  When 
the  tonsil  is  the  source  of  infection,  it  should  be  completely  dissected 
out  as  soon  as  acute  infection  has  passed  off,  in  order  to  prevent  reinfec- 
tion of  the  valves  from  this  source.  The  results  obtained  in  the  Medical 
Clinic  of  the  Johns  Hopkins  Hospital,  where  this  practice  has  been  carried 
out  at  Prof.  Barker's  suggestion,  have  been  very  gratifying.  In  many 
cases  the  recovery  from  the  first  attack  has  been  more  rapid  than  had  been 
usual  before  this  treatment  had  been  resorted  to  (see  page  317),  and  it 
seems  probable  that  reinfection  of  the  valve  is  of  less  frequent  occurrence 
thereafter.  Similar  results  are  seen  in  gonorrhoeal  endocarditis  after  treat- 
ment of  the  urethritis. 

In  these  mild  cases  drug  treatment  may  not  be  absolutely  necessary. 
In  how  far  Cloetta's  suggestion  as  to  the  early  use  of  digitalis  should  be 
carried  out  is  still  unsettled,  but  at  least  the  administration  of  strychnine 
in  doses  of  from  1  to  3  mg.  (eV  to  ^V  g^-)  is  advisable  in  order  to  increase 
the  tonicity  of  the  heart  muscle.  However,  the  blood-pressure  and  hence 
the  strain  upon  the  valves  should  not  be  materially  increased  (not  more 
than  10  mm.  Hg),  and  the  dose  of  strychnine  should  be  reduced  if  it  rise 
above  this  level.    Digitalis  is  not  necessary  in  cases  of  this  type. 

The  bronchitis  which  frequently  accompanies  cases  of  this  type  does 
not  differ  greatly  from  the  ordinary  forms  of  chronic  bronchitis,  and  is 
associated  with  the  usual  pulmonary  bacteria  found  in  these  conditions — 
the  streptococcus,  pneumococcus,  influenza  bacillus,  Friedlander's  bacillus, 
etc.  Treatment  is  therefore  the  same  as  for  ordinary  bronchitis,  a  soothing 
steam  inhalation  being  very  useful.    The  following  are  to  be  recommended : 


Oleum  pini  sylvestris,  or 

Creosoti,  5iss;  5 

Tr.  benzoin,  co., 

Tr.  opii  camphorat.,  aa  oiiss         75 


A  teaspoonful  inhaled  with  steam  from  an  atomizer,  or  from  a  funnel 
above  a  glass  jar  into  which  a  teaspoonful  of  the  remedy  and  a  pint  of 
boiling  water  have  been  placed.  Codein  .015  to  .030  Gm.  (gr.  \  to  h)  or 
heroin  2.5  mg.  (gr.  3V  to  y  2)  "lu-y  be  given  by  mouth  to  relieve  the  cough 
by  reducing  bronchial  secretion  and  irritability. 

Physical  Re=education. — When  the  stage  of  acute  symptoms  has  passed 
the  stage  of  re-education  begins.  The  heart  though  injured  must  be  trained 
to  perform  the  day's  work  without  strain.  To  do  this  the  heart  muscle 
must  be  stronger  than  normal;  it  must  have  hypertrophied.  The  process 
of  hypertrophy  after  valvular  lesion,  like  the  heart  hypertrophy  of  an  athlete 
in  training,  requires  time.  However,  the  amount  of  hypertrophy  setting 
in  after  a  valvular  lesion  is  greater  than  that  after  a  prolonged  period  of 
muscular  exercise,  and  hence  may  be  expected  to  take  a  longer  time.  At 
this  stage  Nauheim  baths  and  resisted  movements  may  be  dispensed  with 
22 


338  DISEASES   OF   THE   HEART   AND    AORTA. 

as  long  as  a  reasonable  supervision  is  kept  over  the  patient.  He  should 
never  be  allowed  to  become  either  very  tired  or  short  of  breath,  and  six 
months  or  a  year  should  elapse  before  he  is  allowed  to  run,  participate  in 
games,  severe  exercise,  or  manual  labor.  The  current  statement  that  the 
prognosis  is  doubtful  during  the  first  year  after  the  occurrence  of  a  valvular 
lesion  is  due  largely  to  the  intercurrence  of  acute  overstrain  of  the  heart 
muscle  before  hypertrophy  is  complete. 

The  condition  is  quite  different,  however,  when  the  mitral  insufficiency 
is  of  long  standing  before  it  is  encountered  by  the  physician,  as  is  frequently 
the  case  in  routine  examinations  for  life  insurance,  civil  service,  etc.  The 
disease  may  then  be  said  to  have  cured  itself  already,  and  beyond  gently 
admonishing  the  patient  against  over-exertion  no  further  precautions  are 
necessary.  It  is  often  unwise  to  inform  a  man  or  woman  of  nervous  tem- 
perament that  a  heart  lesion  is  present,  since  worry  may  in  itself  contribute 
to  the  cardiac  overstrain. 

Cases  of  functional  mitral  insufficiency  are  rarely  devoid  of  cardiac 
symptoms,  and  hence  will  be  considered  under  the  second  group. 

Treatment  of  the  Second  Stage. — The  second  stage  of  mitral  insuffi- 
ciency, in  which  dyspnoea  and  other  symptoms  of  cardiac  origin  are  present, 
represents  a  condition  of  chronic  cardiac  overstrain.  Indeed  it  is  the 
abnormal  severity  of  these  symptoms  following  some  slight  exertion  which 
usually  calls  attention  to  the  existence  of  the  lesion.  The  treatment  does 
not  depart  in  any  essential  particular  from  that  which  has  already  been 
discussed  in  the  case  of  chronic  overstrain  of  the  myocardium.  Just  as  in 
the  milder  cases  the  most  important  element  in  the  treatment  is  absolute 
rest  in  bed,  continued  until  long  after  symptoms  have  subsided.  The 
diet  should  at  first  be  very  light  (see  page  167),  and  should  be  very  gradually 
increased  after  symptoms  have  subsided.  As  in  the  milder  cases,  vigorous 
doses  of  strj'chnine  (2  to  3  mg.  [gr.  -jV  to  2V]  every  four  hours)  should 
be  begun  at  once.  The  bowels  should  be  kept  moving  freely  by  means 
of  Seidlitz  powders,  Epsom  salts,  Hunyadi  water,  Mistura  ferri  aperiens, 
or  some  other  mild  laxative.  It  is  important  that  the  patient  should  sleep 
well  at  night,  and  trional  (1  Gm.=gr.  xv)  or  some  other  soporific  may  be 
given,  if  necessary  with  the  addition  of  codein  (15  mg.  =  gr.  ss).  If  symp- 
toms have  not  diminished  after  a  couple  of  days  of  this  treatment,  digi- 
talis should  be  resorted  to  (see  page  178),  for  it  is  important  not  only  to 
reduce  the  strain  but  also  to  strengthen  the  heart  muscle  as  rapidly  as  pos- 
sible in  order  to  prevent  the  overstrain  from  becoming  permanent.  Indeed 
it  may  be  said  that  this  is  the  all-important  stage  in  the  course  of  mitral 
insufficiency  and  of  all  other  valvular  lesions,  the  stage  which  determines 
whether  the  patient  may  hope  to  return  to  a  life  of  activity  or  must 
look  forward  to  one  of  permanent  invalidism,  and  this  question  is  often 
decided  by  the  promptness  or  tardiness  with  which  the  symptoms  dis- 
appear when  the  patient  is  at  rest.  In  this  stage  the  primary  source 
of  infection  or  reinfection  should  be  treated  just  as  in  the  milder  ones,  but 
the  period  of  rest  should  be  longer  and  the  period  of  physical  re-edu- 
cation and  gymnastics  should  be  very  carefully  undertaken.  The 
more  systematic  methods,  such  as  those  of  Schott,  Herz  and  Oertel,  are 
especially  valuable,  as  are  also  the  Nauheim  baths.    The  important  factor, 


MITRAL   INSUFFICIENCY.  339 

however,  is  that,  whatever  the  method  of  treatment,  the  patient  should 
never  be  allowed  to  become  fatigued  or  short  of  breath,  he  should  be 
gradually  trained  up  to  his  optimum  strength,  and  he  should  never  be 
allowed  to  attempt  to  exceed  his  limit. 

Treatment  of  the  Third  Stage. — In  the  third  stage  of  mitral  insuffi- 
ciency, that  of  broken  compensation,  the  burden  of  the  cardiac  fail- 
ure has  been  shifted  from  the  left  ventricle  to  the  right.  The  treatment 
therefore  follows  the  rules  laid  down  for  broken  compensation  due  to  any 
cause  whatever:  absolute  rest,  immediate  use  of  digitalis  (especially  along 
with  nitroglycerin,  sodium  nitrite,  or  erythrol  tetranitrate) ,  free  purgation, 
and  very  light  diet  being  the  essential  features.  Hypodermic  injections 
of  morphine  (8  to  15  mg.,  gr.  ^  to  \)  may  be  necessary,  but  they  should 
be  used  with  caution,  since  they  decrease  the  irritability  of  the  respiratory 
centre  and  thus  lead  to  accumulation  of  CO2  and  cardiac  asthma.  Since 
many  of  the  symptoms  are  due  to  a  high  pressure  in  the  vena  cava  and 
consequent  dilatation  of  the  right  auricle  and  ventricle,  venesection  is  often 
followed  by  great  improvement,  and  should  be  regarded  as  an  important 
therapeutic  measure  during  the  acute  stage  of  the  overstrain.  But  in 
the  presence  of  anaemia  it  should  not  be  resorted  to.  Intravenous 
strophanthin  (0.5  to  1  mg.)  is  of  the  greatest  value  when  the  symp- 
toms have  become  alarming,  and  should  be  followed  by  the  usual  course 
of  digitalis,  or  by  daily  intramuscular  injections  of  strophanthin. 

As  symptoms  subside,  the  condition  and  its  treatment  pass  into 
those  of  the  second  stage,  and  a  gradual  return  to  normal  may  occur. 
On  the  other  hand  the  symptoms  may  increase,  hydrothorax  and  ascites 
may  become  extensive  and  may  require  tapping,  and  the  oedema  may 
become  extreme.  To  diminish  these  it  may  be  advisable  to  use  diuretics, 
such  as  theobromin  acetate  (agurin),  theocin,  or  acettheocin  sodium,  or 
else  potassium  acetate  and  citrate. 

PROGNOSIS. 

Exactly  how  much  benefit  can  be  effected  by  treatment  varies  with 
each  individual  case,  and  depends  upon  factors  which  are  difficult  to  fore- 
tell. It  is  especially  true  of  mitral  insufficiency  that  while  there  is  life 
there  is  hope,  for  the  patient  may  almost  completely  recover  from  one  or 
more  attacks  of  broken  compensation  and  yet  remaifi  comparatively  free 
from  symptoms  for  a  number  of  years. 

As  regards  the  prognosis  for  the  individual  attack  no  absolute  rule 
can  be  laid  down,  but  much  importance  may  be  attached  to  the  rapidity 
of  change  for  the  better  or  for  the  worse.  A  rapid  improvement  during 
the  first  two  days  may  be  construed  as  favorable  for  the  ultimate  outcome; 
a  slow  recovery  usually  indicates  a  severe  residuum  of  trouble;  an  increase 
of  symptoms  in  spite  of  treatment  is  of  grave  significance. 

Between  attacks  the  patient's  ability  to  hold  his  own  or  even  to  im- 
prove his  condition  depends  entirely  upon  his  ability  to  keep  himself  free 
from  overstrain  and  reinfection.  In  all  cases  the  physician  should  be  some- 
what guarded  in  his  statements  regarding  the  future. 


340  DISEASES   OF   THE   HEART    AND    AORTA. 

BIBLIOGRAPHY. 

Mitral  Insufficiency. 

Krehl,  Geipel.     Quoted  on  page  246. 

Roy  and  Adami:  The  Failure  of  the  Heart  from  Overstrain,  Brit.  M.  J.,  Lond.,  1888,  i, 

1321  and  1395. 
Kulbs.     Quoted  on  p.  212. 
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mitral,  Presse  m6d..  Par.,   1898.     La  region  mitro-aortique;    etude  anatomique  et 

pathologique,  Arch,  de  m6d.  exper.  et  d'anat.  path.,  Par.,  1897,  ix,  235. 
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Valves,  Med.  News,  Phila.,  1884,  xlv,  533. 
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1902,  clxix,  159. 
Gibson,  G.  A.:    Diseases  of  the  Heart  and  Aorta,  Edinb.  and  Lond.,  1898. 
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tone  und  Herzgerausche,  Arch.  f.  d.  ges.  Physiol.,  Bonn,  1908,  cxxiii,  341. 
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1881. 
Gerhardt,  D.:  Ueber  die  Compensation  von  Mitralfehlem,  Arch.  f.  exper.  Pathol,  u.  Pharm., 

Leipz.,  1901,  xlv,  186. 
King,  T.  W.:  An  Essay  on  the  Safety-valve  Function  in  the  Right  Ventricle  of  the  Human 

Heart,  etc.,  Guy's  Hosp.  Rep.,  Lond.,  1837,  ii,  104. 
Osier,  W.,  and  Gibson,  A.  G.:  Modem  Medicine,  Phila.  and  N.  Y.,  1908,  iv,  205. 
Moritz,  F. :  Einige  Bemerkungen  zur  Frage  der  percutorischen  Darstellung  der  gesammten 

Vorderflache  des  Herzens,  Deutsch.  Arch.  f.  klin.  Med.,  Leipz.,  1906,  Ixxxviii,  276. 

Cf.  also  article  by  Dietlen  and  Simon  in  the  same  volume. 
Harris,  Th.:  Some  Clinical  and  Post-mortem  Observations  on  the  Cardiac  Dulnes-i  in 

Cases  of  Mitral  Disease,  etc.,  Med.  Chron.,  Manchester,  1892,  xvii,  287. 
Groedel,  F.  M.:  The  Examination  of  the  Heart  by  the  Roentgen  Rays,  Arch.  Roentg. 

Ray  and  Allied  Phenom.,  Lond.,  1908. 
Hofmann,  Aug.     Quoted  on  p.  119. 
Gerhartz,  H.:  Zur  Frage  des  Stethoskops,  Deutsch.  Arch.  f.  klin.  Med.,  Leipz.,  1907,  xc, 

501. 
Naunyn,  B.:  Ueber  den  Grund  weshalb  hin  und  wieder  das  systolische  Geriiusch  bei  der 

Mitralinsufficienz  am  lautesten  in  der  Gegend  der  Pulmonalklapp  zu  vernehmen  ist, 

Berl.  klin.  Wchnschr.,  1868,  v,  189. 
Boy-Teissier:  L'auscultation  retrostemale,  Rev.  de  Med.  Paris,  1892,  xii,  169. 
Wild,  R.:  A  Contribution  to  the  Pathology  of  the  Coronary  Arteries,  Med.  Chron.,  Man- 
chester, 1892,  xvi,  223. 
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kulose,  Ztschr.  f.  Tuberk.,  etc.,  1902,  iii,  378. 


III. 

MITRAL  STENOSIS. 

HISTORICAL. 

After  mitral  insufficiency  the  most  common  affection  of  the  mitral 
valve  is  that  which  leads  to  mitral  stenosis.  This  condition  was  first  de- 
scribed by  John  Mayow  in  1669  in  the  case  of  a  young  man  who  died  after 
several  years  of  dyspnoea,  palpitation,  and  attacks  of  syncope,  "  At  autopsy 
he  found  dilatation  and  hypertrophy  of  the  right  ventricle  and  almost 
complete  closure  of  the  left  auriculoventricular  orifice  by  a  'cartilaginous 
product, '  so  that  the  blood  could  scarcely  traverse  the  left  ventricle  and 
was  compelled  to  flow  backward  to  the  pulmonary  vessels,  hence  the  disten- 
tion of  the  right  ventricle."  Vieussens  (1715)  described  similar  findings, 
noting  also  that  the  papillary  muscles  were  changed  to  small  short  tendons, 
and  that  the  right  ventricle  was  so  dilated  as  to  allow  reflux  of  blood  past 
the  tricuspid  valve.  He  further  noted  weakness  and  irregularity  of  the 
pulse,  and  ascribed  it  to  ''too  small  quantity  of  blood  which  the  left  ven- 
tricle furnished  to  the  aorta  .  .  .  and  the  irregularity  of  its  contrac- 
tions." Senac  (1749)  and  others  described  cases,  so  that  the  lesion  became 
quite  familiar  to  pathologists  in  the  early  part  of  the  nineteenth  century. 


PATHOLOGICAL   ANATOMY    AND    PATHOGENESIS. 

Pathologically,  it  is  brought  about  by  a  chronic  inflammatory  process 
taking  place  in  the  tissue  of  the  valve  which  leads  to  thickening  and  fusion 
of  the  cusps.  By  this  fusion  the  valve  comes  to  form  a  sort  of  funnel,  some- 
times elongated,  sometimes  short 
and  shallow.  The  walls  are  much 
thicker  than  those  of  the  normal 
valve,  owing  to  a  chronic  infiltra- 
tion and  proliferation  of  the  con- 
nective tissue  within  them.  They 
are  usually  more  or  less  rigid,  some- 
times smooth,  sometimes  rough  from 
remains  of  old  vegetations  and  calci- 
fications, and  the  auricular  surface 
is  often  puckered  or  thrown  into 
folds.  The  lower  margin  of  the 
valve  is  attached  to  the  chordae 
tendineae,  which  become  shortened 

and  thickened  very  early  in  the  process.  The  orifice  thus  formed  is 
sometimes  circular,  sometimes  oval  or  button-holed,  sometimes  irregular 
(Fig.  189).     According  to  Sansom,  the  funnel  shape  is  more  common  in 

341 


Fig.  189.  —  Human  liean,  r.iiuv\iiig  mitral  (Af) 
and  tricuspid  (T)  stenosis.  Viewed  from  above. 
The  auricles  ha\  e  been  cut  through. 


342  DISEASES   OF   THE   HEART    AND    AORTA. 

children,  while  the  buttonhole  is  more  common  in  adults  and  represents 
a  lesion  of  longer  duration.  The  orifice  may  often  become  veiy  small 
before  death  ensues,  sometimes  barely  large  enough  to  admit  a  goose-quill 
(Sansom).  In  some  long-standing  lesions  the  margin  of  the  valve  may 
become  so  thick  and  stiff  (sometimes  calcified,  cartilaginous,  or  ossified) 
that  it  does  not  close  during  ventricular  systole;  in  others  the  edges 
become  retracted  so  that  they  no  longer  cover  the  orifice.  In  either  case 
secondary  mitral  insufficiency  may  result. 

Occurrence. — According  to  the  studies  of  Lockhart  Gillespie,  mitral 
stenosis  is  most  common  in  women,  increasing  in  frequency  up  to  the 
age  of  29.  In  men  it  is  scarcely  more  than  half  as  common,  but  reaches 
its  maximum  frequency  a  decade  later.  The  males  affected  die  earlier  than 
the  females,  however;  the  average  period  of  death  being  from  30  to  39  with 
the  former,  while  with  the  latter  it  is  40  to  49.  The  presence  of  the  double 
mitral  lesion  does  not  shorten  the  average  period  of  life. 

Etiology. — As  regards  etiology,  Cheadle,  Samways,  Duroziez,  and 
Dyce  Duckworth  agree  that  rheumatism  is  the  etiological  factor  in  at 
least  60  per  cent,  to  78  per  cent,  of  the  cases,  other  acute  infections,  chlo- 
rosis (Goodhart),  chronic  nephritis,  gout,  arteriosclerosis,  and  puerperal 
infections  representing  the  other  etiological  factors.  Potain  also  believes 
that  pulmonary  tuberculosis  is  an  important  factor,  but  this  is  disputed 
by  many  writers;  most  of  whom  agree  with  Traube  that  tuberculosis  is 
far  less  frequent  (5  per  cent.)  in  the  presence  of  mitral  stenosis  than  in 
normal  individuals  (12  per  cent.)  or  in  those  with  other  heart  lesions 
(Meisenburg,  Tileston). 

Pathogenesis. — As  regards  pathogenesis,  Huchard  (I.e.)  divides  the 
cases  of  mitral  stenosis  into  three  groups : 

1.  The  congenital  form,  resulting  from  fetal  endocarditis,  which, 
as  Sansom  has  shown,  is  very  rare. 

2.  The  endocarditic  form  of  infectious  origin  (due  especially  to 
rheumatism,  scarlet  fever,  measles,  typhoid  fever,  smallpox,  etc.),  resulting 
from  the  organization  and  fusion  of  old  vegetations.  This  is  the  most  com- 
mon form,  since  rheumatism  alone  can  be  demonstrated  as  an  etiological 
factor  in  about  70  per  cent,  of  the  cases. 

3.  The  sclerotic  form,  which  is  associated  with  general  arterio- 
sclerosis, gout,  and  plumbism.  In  this  group  no  traces  of  endocarditic  vege- 
tations occur  upon  the  valve,  and  the  process  is  more  closely  allied  to  that 
within  the  vessel  walls  in  arteriosclerosis.  Under  this  group  should  also  fall 
the  large  group  of  cases  associated  with  chlorosis  and  other  anaemias  in 
which  no  other  causal  factor  is  present  to  explain  the  presence  of  the  lesion. 
Goodhart,  who  lays  especial  stress  upon  this  group,  believes  that  the 
chronic  overstrain  of  the  anaemic  heart  muscle  is  followed  by  oedema 
and  petechias  in  the  substance  of  the  mitral  valve,  as  has  been  demonstrated 
experimentally  by  Roy  and  Adami.  He  thinks  that  this  oedema  is  followed 
by  cellular  infiltration  and  finally  by  proliferation  of  fibrous  tissue  resulting 
in  the  mitral  stenosis.  While  this  view  is  suggestive,  no  careful  histological 
or  experimental  studies  have  been  made  to  bear  it  out.  On  the  other  hand, 
it  must  be  remembered  that  most  anaemic  and  gouty  persons  are  subject  to 
repeated  slight  infections  which  might  suffice  to  produce  chronic  changes  in 


MITRAL  STENOSIS. 


343 


the  heart  during  the  lapse  of  years.  Weber  and  Deguy  have  shown  that 
hemorrhage  occurs  often  in  the  valves  after  labor,  etc.  This  is  followed 
by  infiltration  and  organization  and  finally  by  sclerosis  of  the  valve. 


PATHOLOGICAL    PHYSIOLOGY. 

The  nature  of  the  disturbance  to  the  circulation  in  mitral  stenosis  was 
already  discerned  by  Vieussens  in  1715,  who  noted  that  owing  to  the  inabil- 
ity of  the  blood  to  pass  through  the  mitral  orifice  with  sufficient  rapidity, 
it  had  become  dammed  back  in  the  pulmonary  veins  and  pulmonary  arte- 
ries, increasing  the  work  of  the  right  ventricle  and  leading  to  insufficiency  of 
the  tricuspid  valve.  At  the  same  time  the  force  of  the  pulse  (blood-pressure) 
and  amplitude  of  the  pulse  were  diminished,  owing  to  the  diminution  of  the 
blood  which  entered  or  was  forced  out  of  the  left  ventricle.  Vieussens 
noted  further  that  the  force  and  rhythm  of  contraction  were  irregular. 


I 

NORMAL 

II 

BROKEN 

PULMONARY 

COMPENSATION 

III 

BEGINNING 

FAILURE  OF  LEFT 

VENTRICLE 

AO 

AO 

M»X^ 

MW^                                                                       / 

,, 

-A 

MIN^^^                                                     / 

.Jj2                           , 

^ 

1              \              K.                              1 

"'"i^              PA 

\ 

1               \            ^^^                     ' 

/A    ^-     ' 

V  ^ 

1                   \      /^^^"^^ 

'     \  / 

^^ 

\^                ^-OA 

\^ 

M 

t 

t»»t«« 

'''*^^      ^ 

.»e^.,^  .. 

pm 

1 

fm^ 

Fig.  190. — Diagram  showing  the  changes  in  the  circulation  due  to  mitral  stenosis.  The  stage  of 
perfect  compensation  is  not  shown,  since  there  are  practically  no  pressure  changes.  II  represents  the 
stage  at  which  pulmonary  compensation  is  broken  but  systemic  circulation  has  not  yet  become  aflfected. 
Ill  represents  the  stage  in  which  there  is  broken  pulmonary  compensation,  and  the  left  ventricle  has  failed 
to  maintain  the  arterial  pressure.  The  last  pressure  changes  in  the  last  stage,  with  broken  systemic  com- 
pensation as  well,  correspond  exactly  to  those  in  the  last  stage  of  mitral  insufficiency. 

The  changes  of  pressure  corresponding  to  these  phenomena  have  been  studied  experi- 
mentally by  Bettelheim  and  Kauders,  D.  Gerhardt,  and  MacCallum  and  McClure,  who  have 
found  that  the  production  of  a  mild  grade  of  experimental  stenosis  causes  distinct  rise 
in  the  mean  pressure  within  the  left  auricle,  the  pulmonary  veins 
and   the  pulmonary  artery. 

Filling  of  the  Ventricles. — The  effect  of  the  stenosis  upon  the  filling 
of  the  ventricles  as  shown  in  the  volume  curve  has  recently  been  investi- 
gated by  the  writer,  aided  by  Mr.  J.  M.  Wolfsohn.  As  shown  in  Fig.  191, 
the  first  effect  of  the  mitral  stenosis  is  to  slow  the  inflow  into  the  left  ven- 
tricle. As  a  result  of  this  the  left  auricle  is  more  than  usually  full  at  the 
time  of  its  systole,  and  forces  an  unusually  large  quantity  of  blood  into  the 
ventricle  (Fig.  192,  as).  This  increase  in  auricular  output  at  first  suffices 
to  complete  the  filling  of  the  ventricle,  but  as  the  lesion  progresses  a  little 
further  even  this  fails  to  do  so  and  the  amount  of  blood  entering  the  ven- 
tricle falls  below  normal.     As  a  consequence  of  this,  the  ventricle  forces 


344 


DISEASES   OF   THE    HEART    AND    AORTA. 


less  blood  into  the  aorta,  the  arterial  blood-pressure  falls  and  the  pulse- 
pressure  diminishes.  This  is  the  condition  as  observed  in  the  experiment. 
In  man,  however,  where  the  pathological  change  is  a  gradual  one,  the 
arteries  gradually  accommodate  themselves  by  constriction  of  their  chan- 
nels until  the  blood-pressure  has  returned  to  about  its  normal  level. 
The  pressure  in  the  systemic  veins  is  diminished,  as  has  been  shown  by 
Kornfeld. 

LIGATURE  TIGHTENED 


VOL. 


CAR. 


Fig.  191. — Volume  of  the  ventricles  in  experimental  mitral  stenosis.  (Kindness  of  the  Johns 
Hopkins  Hospital  Bulletin.)  Tracings  obtained  from  a  dog's  heart  in  experimental  mitral  stenosis. 
VOL.,  volume  curve;  CAR.,  carotid  pressure.  The  arrow  indicates  the  moment  at  which  the  stenosis 
was  produced.  The  filling  of  the  ventricles  (downstroke)  was  slowed,  diastasis  (horizontal  part  of  curve) 
sets  in  prematurely,  and  the  part  of  the  curve  due  to  auricular  systole  (second  downstroke)  becomes 
more  pronounced.     The  heart  rate  is  practically  unchanged. 


S         D 
NORMAL 

Fig.  192. — Diagram  illustrating  the  variations  in  the  volume  curve  of  the  ventricles  in  increasing 
degrees  (I,  II,  III,  IV)  of  mitral  stenosis.  S,  systole;  D,  diastole,  AS,  inHow  into  the  ventricles  due  to 
systole  of  the  auricles. 

As  the  narrowing  of  the  mitral  orifice  progresses,  a  further  change 
occurs  in  the  filling  of  the  heart.  It  now  requires  a  greater  difference  in 
pressure  to  drive  the  blood  from  auricle  to  ventricle  and  as  a  consequence 
it  is  seen  that  during  a  great  part  of  diastole  little  or  no  blood  is  flowing  in. 
Diastole  is  thus  divided,  according  to  Henderson's  terminology  (cf.  page 
9),  into  three  periods: 

I.  A  period  of  eariy  diastole,  during  which  the  ventricle  fills  with  moderate  rapidity, 

though  more  slowly  than  normally. 
II.  A  period  of  diastasis  (Henderson),  during  which  little  or  no  filling  occurs.  Experi- 
ments upon  the  excised  heart  (cf.  page  9)  indicate  that  the  mitral  valves  close 
suddenly  just  at  the  beginning  of  this  period  and  remain  completely  or  almost 
completely  closed  until  the  next. 
III.  This  is  followed  by  the  third  event  of  diastole,  when  more  blood  is  driven  into  the 
ventricle  by  the  forcible  contraction  of  the  left  auricle.  The  latter  must  now  con- 
tract more  forcibly  than  ever  and  as  a  consequence  hypertrophies.  Indeed  Ger- 
hardt  has  shown,  from  the  autopsies  of  two  cases  with  very  mild  grades  of  stenosis, 
that  hypertrophy  of  the  left  auricle  is  the  first  change  resulting  from  the  lesion, 
and  that  hypertrophy  of  the  right  ventricle  is  a  later  phenomenon.  Pulmonary 
congestion  always  occurs,  however,  and  in  all  but  the  very  mildest  cases  hypertrophy 
of  the  right  ventricle  results. 


MITRAL   STENOSIS.  345 

With  further  narrowing  the  filUng  of  the  left  ventricle  diminishes,  its 
total  volume  and  systolic  output  diminish,  and  the  blood-pressure  falls 
unless  the  constricting  power  of  the  vasomotor  is  taxed  to  the  utmost  to 
preserve  it.  The  left  auricle,  on  the  other  hand,  becomes  overloaded  and 
distended,  its  capacity  even  rising  from  60  c.c.  to  2500  c.c.  (G.  Miiller)  or 
3000  c.c.  (Minkowski).  Under  these  circumstances  paralysis  of  the 
auricle  sets  in,  the  auricular  wave  disappears  from  the  curve  of 
filling  (Hirschf elder) ,  from  the  jugular  pulse  (Mackenzie),  and  the  oesoph- 
ageal tracing  (Joachim),  and  the  presystolic  rumble  is  no  longer 
heard.  At  this  stage  the  rhythm  of  the  heart  usually  becomes  irregu- 
lar, due  no  doubt  to  the  effort  of  the  auricle  to  empty  itself  by  means  of 
abnormal  contractions.  This  stage  of  irregularity  with  auricular  paralysis 
is  more  or  less  characteristic  of  cardiac  overstrain  in  mitral  stenosis,  and 
may  disappear  when  the  work  of  the  heart  is  relieved,  or  its  strength  is 
increased  by  digitalis  (see  Fig.  199),  when  the  presystolic  rumble 
reappears.  As  the  lesion  progresses  further,  the  stasis  in  the  pulmo- 
nary circulation  increases,  and  broken  compensation  follows,  just  as  it 
does  in  mitral  insufficiency. 

As  can  be  seen  from  the  above  description,  the  problem  of  maintain- 
ing compensation  in  mitral  stenosis  is  quite  different  from  that  in  mitral 
insufficiency.  In  the  latter  condition  the  important  factor  was  seen  to  be 
the  emptying  of  the  left  ventricle,  whereas  in  mitral  stenosis  the 
difficulty  lies  in  the  filling  of  this  chamber,  and  the  hypertrophy 
necessary  to  bring  this  about  affects  not  the  left  but  the  right  ven- 
tricle and  the  left  auricle.  Since  this  can  be  accomplished  only  by  increas- 
ing the  pulmonary  engorgement,  it  is  evident  that  after  the  lesion  has 
reached  a  certain  stage  perfect  compensation  becomes  impossible,  and  the 
re-establishment  of  compensation  is  always  more  difficult  than  in  a  corre- 
sponding grade  of  mitral  insufficiency. 

SYMPTOMS    AND    SIGNS. 

The  symptoms,  color,  and  general  appearance  of  patients  with  mitral 
stenosis  are  very  much  the  same  as  in  those  with  mitral  insufficiency, 
except  that  they  are  somewhat  more  pronounced  and  more  persistent. 
Haemoptysis  and  precordial  pain  are  more  frequent  than  in  mitral  insuffi- 
ciency, as  are  also  attacks  of  pulmonary  oedema. 

Hofbauer,  Alexander,  Miecslaw,  Frischauer,  and  Osier  have  called 
attention  to  the  hoarseness  and  stenotic  (brassy)  cough  as 
a  symptom  in  mitral  stenosis.  Osier  has  shown  at  autopsy  that  under 
these  conditions  the  left  recurrent  laryngeal  nerve  is  compressed  against 
the  arch  of  the  aorta  and  the  ligamentum  Botalli  by  the  dilated  left  auricle, 
and  then  undergoes  degenerative  changes. 

Andr6  Petit  recognizes  three  clinical  groups  of  persons  with  mitral  stenosis: 
I.  The  c  h  1  o  r  o  t  i  c  type  affecting  mainly  young  girls.  The  skin  and  mucous  mem- 
branes are  pale,  the  complexion  sallow.  The  patients  readily  become  short  of 
breath,  are  subject  to  nose-bleeds,  menstrual  disturbances,  dyspepsia,  constipation, 
and  nervousness.  Only  auscultation  reveals  the  nature  of  the  disease. 
II.  The  pseudotuberculous  type  in  young  women,  characterized  by  repeated 
attacks  of  bronchitis,  dry,  hacking  cough,  and  hsemoptysis,  especially  at  menstrual 


346 


DISEASES   OF   THE   HEART   AND    AORTA. 


periods.  The  patients  are  pale  and  emaciated  and  closely  resemble  consumptives 
in  appearance. 
III.  The  dyspnoeic  type  into  which  any  of  the  other  types  may  merge.  There  is 
dyspnoea  on  exertion,  frequently  also  attacks  of  cardiac  asthma  at  night.  These 
patients  usually  have  flushed  faces,  with  slight  dull  tinge  of  cyanosis  (the  typical 
mitral  facies),  due  to  imperfect  aeration  of  the  blood  in  the  lungs. 


PHYSICAL    EXAMINATION. 

Except  for  the  findings  in  the  immediate  vicinity  of  the  heart,  the 
results  of  physical  examination  in  cases  of  mitral  stenosis  are  practically 
the  same  as  in  mitral  insufficiency.  The  pulse,  however,  is  rarely  of  as 
long  volume  as  in  the  latter,  and  the  pulse-pressure  is  usually  smaller. 
Irregularity  is  about  as  common  and  is  of  the  same  type  (absolute  irregular- 
ity, with  or  without  auricular  paralysis)  in  both  conditions. 

The  Cardiac  Impulse. — The  findings  about  the  heart  are,  however, 
characteristic.  The  apex  impulse,  sometimes  in  the  normal  position  and 
sometimes  out  in  the  axilla,  is  usually  well  marked,  sudden,  short,  and 
tapping  or  flapping.  This  peculiar  appearance  is  due  to  the  seesaw  move- 
ments of  the  chest  wall  over  the  right  and  left  ventricles.  There  is  a  wavy 
movement  in  the  third,  fourth,  and  fifth  interspaces,  which  when  accurately 

timed  or  recorded  is  found  to  consist  of  a  systolic 
retraction  of  these  interspaces  over  the  hyper- 
trophied  right  ventricle  (see  page  209).  The 
systolic  impulse  of  the  pulmonary  artery  may 
sometimes  be  seen  in  the  second  left  interspace 
at  the  sternal  margin. 

Palpation.  —  The  findings  of  palpation  are 
perfectly  characteristic.  At  the  apex,  and 
usually  over  this  area  only,  the  shock  of  the 
first  sound  can  be  felt,  short,  sharp,  and  tap- 
ping. In  the  typical  cases,  up  to  the  last  stage 
(auricular  paralysis)  this  is  preceded  by  a  short 
presystolic  thrill,  having  9,  "purring"  character 
(fremissement  cataire,  Corvisart,  Laennec), 
leading  up  to  the  shock  which  accompanied  the 
first  sound.  It  can  be  increased  by  slight 
exercise.  It  is,  as  a  rule,  sharply  localized 
about  the  apex  in  an  area  of  about  3  cm.  in 
diameter  (or  about  the  size  of  a  stethoscope  bell),  probably  because  it  is 
produced  by  the  impact  of  the  narrow  stream  driven  by  the  forcible 
auricular  contraction  directly  against  the  apical  portion  of  the  walls  of 
the  left  ventricle. 

Indeed  Oestreich,  Lenhartz,  and  Burk  have  shown  that  this  stream  may  finally  cause 
a  bulging  of  the  ventricular  wall  at  the  point  where  it  has  been  striking.  The  vibra- 
tions transmitted  from  the  chordse  tendinese  and  papillary  muscles  are  also  factors  in  its 
production. 

Occasionally  a  tap  or  thrill  is  also  to  be  felt  in  early  or  m  i  d  -  d  i  a  - 
stole  accompanying  the  third  heart  sound  or  the  diastolic  rumbles 
about  to  be  described.  The  sensation  thus  imparted  by  the  presystolic 
thrill  and  the  tapping  first  shock  are  so  characteristic  that  the  diagnosis 


Fig.  193. — Diagram  showing  the 
direction  of  the  stream  entering 
the  left  ventricle  through  the  ste- 
notic mitral  orifice. 


MITRAL  STENOSIS. 


347 


of  mitral  stenosis  may  often  be  established  from  palpation  alone.  The 
shock  accompanying  the  second  sound  is  usually  very  distinct,  and  becomes 
markedly  accentuated  as  the  pulmonary  area  is  approached. 

Percussion. — The  typical  area  of  dulness  on  percussion  and  the  cardiac 
outline  as  seen  by  the  X-ray  (Groedel)  often  show  the  outline  of  the  left 
ventricle  (lower  border  and  lower  half  of  left  border)  to  be  normal,  though 
in  almost  equal  frequency  it  is  extended  to  the  left.  Thus,  in  32  cases 
Sansom  found  the  left  ventricle 

Normal  in 12 

Hypertrophied  in 9 

Dilated  in 5 

Dilated  and  hypertrophied  in .  .   3 

Small  in 3 

Thin  walled  in 1 

Above,  the  area  of  dulness     ^^m  i  ^\^ 

extends  higher  and  further  to     ^^H  \  I      "y"  ]      /        /y^v 

the    left    than    normal,    often     ^^^  *0 f J-L 

reaching  as  high  as  the  second 
rib  (though  usually  not  above 
the  third)  and  embracing  an  area 
of  2  to  5  cm.  in  the  second  left 
interspace. 

As  shown  by  the  autopsies  of  Th.  ,._    ,„,       „     .  ,  j    .   .,  ■    ^-        ,  ^, 

,.             •'         J     J    T  f  lo-  19*-  —  Cardiac  oiiiline  and  distribution  of  the 

Hams,     this     area     Ot     dulness     COrre-  presystolic  rumble  in  mitral  stenosis.     The  area  of  cardiac 

spends      to      the      dilated      COnus  dulness  is  indicatetl  by  a  light  line,  the  cardiac  flatness  by 

arteriosus  and  dilated  pulmonary  a  heavy  line.     The  area  over  which  the  presystolic  rum- 

,                 J          i     i        iu         1-1    i    J     1   rl  b'e  and  snapping  first  sound  are  heard  is  indicated  bv  a 

artery    and     not     to     the     dilated     left  ^.i^ele.     The  relation  of  these  sounds  to  the  cardiac  cycle 

auricle.      Except    when    general  failure  is  shown  in  the  small  diagram  at  the  left.     The  systolic 

has    set    in,   the    right    border    of    the  retraction   over  the  right  ventricle  is  indicated  by  the 

heart  is  normal,  but  the  cardiac  flat-  '""''^''^  cardiogram, 
ness  may  be   increased  and  reach  to 

the  right  sternal  margin  (hypertrophy  of  the  right  ventricle).  The  typical  area  of  cardiac 
dulness  in  mitral  stenosis  is  therefore  a  short,  wide  oval  with  a  bulging  upon  its  upper 
left  margin  (Fig.  194). 

Auscultation. — Presystolic  Rumble. — The  auscultatory  findings  in  mitral 
stenosis  are  quite  unique,  and  usually  furnish  the  basis  for  diagnosis.  The 
characteristic  sign  is  a  rumbling  or  echoing  sound  in  late  diastole  (auriculo- 
systolic  in  time),  increasing  in  crescendo  up  to  the  beginning  of  the  first 
heart  sound.  Like  the  presystolic  thrill  and  the  diastolic  sounds,  this 
presystolic  rumble  is  usually  heard  over  an  area  of  2-3  cm.  only,  at  or  a 
little  to  the  right  of  the  apex. 

The  rumble  and  the  first  sound  thus  come  to  have  the  phonetic  equivalent  of  Trup, 
tr-rr-rup,  Turrup  (Steel),  Rou  fut  (Duroziez).  It  was  first  described  by  Gendrin  in 
1842  and  by  Fauvel  in  1843  in  cases  of  mitral  insufficiency,  but  its  diagnostic  significance 
was  definitely  established  by  W.  T.  (jairdner,  of  Edinburgh,  in  1861.  Gairdner  and  the 
older  writers  considered  it  to  be  produced  by  systole  of  the  left  auricle  (auricular-systolic) 
driving  the  blood  forcibly  through  the  narrow  mitral  orifice.  This  view  has  been  practi- 
cally proved  by  the  observations  of  James  Mackenzie  that  the  presystolic  murmur  is  present 
only  when  the  venous  tracing  shows  contractions  of  the  auricles,  and  disappears  when  the 
auricle  becomes  paralyzed.  Joachim  has  also  demonstrated  this  for  the  left  auricle  by 
CBSophageal  tracings.  The  writer  (I.  c),  moreover,  has  been  able  to  demonstrate  this 
parallelism   in   experimental     mitral     stenosis.     Einthoven's   curves    of   the 


348 


DISEASES   OF   THE   HEART    AND    AORTA. 


heart  sounds  in  man,  as  well  as  those  of  Weiss  and  Joachim,  also  prove  the  time  of  its 
occurrence.  It  is  quite  certain,  therefore,  that  the  rumble  does  not  occur  in  the  early  part 
of  ventricular  systole,  as  claimed  by  Ormerod,  Barclay,  Turner,  Dickinson,  and  Brockbank. 
The  protodiastolic  and  mid-diastolic  rumble  remains,  however,  in  spite  of  auricular  paralysis. 


Fig.  195. — Radiograph  from  a  case  of  mitral 
stenosis,  taken  with  the  plate  behind  the  patient, 
showing  increase  of  the  shadow  due  to  the  dilated 
left  auricle.  (Kindness  of  Prof.  C.  M.  Cooper.)  The 
left  ventricle  is  not  dilated. 


Fig.  196. — Diagram  representing  the  shadows 
shown  in  Fig.  195.  The  broken  line  indicates  the 
outline  of  a  normal  heart.  The  arrow  indicates  the 
enlargement  upward  in  the  transvere  oblique  diam- 
eter. LA,  left  auricle;  PA,  pulmonary  artery; 
AO,  aorta;  LV,  left  ventricle. 


Snapping  First  Sound.  —  The  nature  of  the  first  heart  sound  is  also  char- 
acteristic. It  is  short  and  sharp,  and  may  resemble  the  second  sound  so 
closely  as  to  be  mistaken  for  the  latter.  This  is  especially  common  in 
cases  in  which  the  second  sound  is  not  well  heard  at  the  apex. 

Fenwick  and  Overend  believed  that  it  was  of  higher  pitch  than  the  normal  first  sound, 
but  this  is  not  borne  out  by  the  curves  of  Weiss  and  Joachim,  who  found  waves  of  about 
normal   pitch   but   of  much    greater    amplitude    (Fig.  197).      It   is   possible 

that    Fenwick   and    Overend    may 


P    1 


P    1 


CAROTID 


SOUND 


have  heard  higher  overtones  than 
accompany  the  normal  heart  sound. 
Owing  to  its  loudness  and  sharp- 
ness, it  may  so  closely  resemble  the 
normal  second  sound  as  to  be  mis- 
taken for  it.  According  to  Haycraft, 
it  is  the  valvular  element  which 
imparts  the  high-pitched  notes  to 
the  first  sound,  and  this  is  naturally 
accentuated  in  mitral  stenosis,  for 
the  stiff  mitral  valve  plays  a 
greater  role  in  sound  production 
than  in  the  normal. 

Broadbent  and  Acland  be- 
lieved that  the  ventricular  walls 
"  close  down  rapidly  because  their  cavity  is  not  distended  with  blood "  and  thus  give  rise 
to  a  more  sudden  sound.  However,  the  snapping  sound  is  quite  as  pronounced  in  the 
numerous  cases  in  which  the  ventricle  is  dilated;  and  moreover,  on  the  other  hand,  the 
cardiometer  shows  that  diminution  in  ventricular  volume  occurs  at  exactly  the  same  rate 
as  in  the  normal  heart.' 


Fig.  197. —  Graphic  record  of  carotid  puLse  and  heart 
sounds  in  mitral  stenosis.  (After  Weiss  and  Joachim.)  Upper 
line,  carotid  pulse ;  middle  line,  phonogram ;  lower  line, 
time  in  tbo  seconds ;    P,  presystolic  rumble;  1,  2,  heart  sounds. 


*  On  account  of  the  smaller  amount  of  blood  discharged  at  the  usual  rate,  the  dura- 
tion of  systole  is  shorter;  but  Einthoven's  tracings  show  that  the  duration  of  the  first  sound 
is  normal. 


MITRAL   STENOSIS. 


349 


This  applies  only  to  the  first  sound  produced  in  the  left  ventricle, 
and  hence  heard  only  over  a  small  area  about  the  apex  from  which  it  is 
transmitted  for  a  short  distance  upward  and  to  the  right.  Over  the  right 
ventricle  the  first  sound  is  normal  until  the  latter  stages  of  the  disease, 
when  it  is  often  replaced  by  the  murmur  of  tricuspid  insufficiency.  The 
second  sound  at  the  apex  is  usually  faint,  and  may  even  become  quite 
inaudible  in  the  latter  stages  of  the  disease,  probably  owing  to  the  low 
arterial  blood-pressure,  but  over  the  pulmonic  area  it  is  markedly  accen- 
tuated. 


INTRAVENTRICULAR 
PRESSURE 


VENTRICULAR    3 
VOLUME    ^h 
CURVES 

I 


SOUNDS 
CORRESPONDING  TO 

VOLUME    2 
CURVES 


Fig.  198. — Diagram  showing  the  relations  of  the  various  sounds  heard  in  uncomphcated  mitral 
stenosis  to  events  in  the  filling  and  emptying  of  the  ventricle.  N,  normal.  Light,  heavy,  broken,  and  dot- 
ted lines  correspond  with  sounds  whose  base  lines  are  made  with  these  lines. 


Digital  Imitation  of  the  Presystolic  Rumble  and  Snapping  First  Sound. — While  the 
ordinary  vowel  and  consonant  sounds  fail  to  give  any  close  imitation  of  the  sounds  heard 
in  mitral  stenosis,  these  may  be  quite  closely  reproduced  by  the  method  of  H.  L.  Smith 
(page  115),  tapping  on  the  knuckles  with  four  fingers  in  rapid  succession. 

Systolic  Murmur  in  Mitral  Stenosis  with  Mitral  Insufficiency. — Since  the  mitral  cusps 
are  much  deformed  and  thickened  in  mitral  stenosis,  and  the  chordae  tendinese  shortened, 
it  is  not  surprising  that  leakage  at  this  valve  should  be  present  in  the  greater  number  of 
cases  (Fig.  179).  The  group  of  signs  due  to  the  insufficiency  of  the  valve  associated  with 
stenosis  do  not  present  striking  differences  from  the  signs  of  the  former  lesion  when  existing 
alone.  Hypertrophy  of  the  left  ventricle  occurs  in  almost  all  these  cases,  and  the  heart  is 
enlarged  horizontally  to  the  left.  A  blowing  systolic  murmur  accompanies  and  follows  the 
snapping  first  sound;  and  occasionally,  when  the  second  sound  at  the  apex  is  absent  or 
very  soft,  this  murmur  may  seem  to  be  diastolic.  Careful  timing  by  comparison  with  the 
shocks  and  the  time  of  the  pulmonic  second  sound,  however,  will  prevent  this  error. 


350 


DISEASES   OF   THE   HEART    AND    AORTA. 


Sounds  in  Early  and  Mid=diastoIe. — The  sounds  heard  in  early  and  mid- 
diastole,  however,  are  quite  as  well  marked  as  is  the  presystolic  murmur. 
These  sounds  are  of  three  types: 

1.  An  early   diastolic  sound,  the  third    s  o  u  n  d  of  a  proto- 

1  2  3 

diastolic  gallop  rhythm  (rup  -  tat  -  ta) ,  which  Bouillaud  observed  in  1841 
in  association  with  mitral  stenosis.  This  sound  is  heard  in  about  65  per 
cent,  of  all  cases  of  mitral  stenosis  (Steell).  Though  somewhat  louder  it 
does  not  seem  to  differ  from  the  third  sound  of  the  normal  heart  in  mode 
of  production,  and  is  probably  due  to  the  sharp  closure  of  the  mitral  cusps 
when  the  period  of  rapid  ventricular  filling  has  come  to  an  end.  It  is  there- 
fore to  be  regarded  as  a  "closing  snap"  of  the  mitral  (Hirschfelder,  I.e.), 
and  not  as  an  "opening  snap"  as  thought  by  Duroziez,  Sansom,  and  Potain. 
As  the  filling  of  the  ventricle  is  somewhat  less  complete  than  normal,  this 
sound  occurs  a  trifle  early  (Thayer).  That  it  should  be  louder  and  more 
readily  produced  is  due  to  the  rigidity  of  the  altered  mitral  valve. 


2.5  1.8         1.7       2.0  2.5  2.6 


Fig.  199. — Venous  pulse  of  a  patient  with  mitral  stenosis  during  an  attack  of  acute  heart  failure. 
A.  Tracing  taken  on  Dec.  -1,  1907.  The  presystolic  rumble  has  disappeared.  The  a  (auricularl  wave  is 
absent  from  the  venous  pulse.  There  is  absolute  arrhythmia.  B.  Tracing  taken  five  days  later,  after 
return  of  compensation.  The  presystolic  rumble  has  returned;  the  a  wave  is  present  on  the  venous  pulse. 
The  rhythm  is  regular.     The  arrows  mark  the  time  when  auricular  contraction  should  occur. 


2.  One  of  the  commonest  sounds  in  mitral  stenosis  is  a  rumble 
in  early  or  in  mid-diastole  of  the  same  character  as  the  pre- 
systolic rumble.  According  to  fluchard,  it  may  resemble  the  sound  of  a 
flag  fluttering  in  the  breeze,  causing  the  cardiac  cycle  to  resemble  the  words 

"rup  -  tat  -  rarou."  This  rumble  may  follow  almost  immediately  after 
the  second  sound.  It  may  last  throughout  diastole  and  be  continuous 
with  the  presystolic  rumble,  or  it  may  be  separated  from  the  second  sound 
and  also  from  the  presystolic  by  short  intervals.  On  the  other  hand,  when 
the  presystolic  rumble  has  disappeared  during  auricular  paralysis  it  may  be 
the  only  sound  heard  during  diastole. 

These  rumbles  occur,  therefore,  at  the  time  when  the  blood  is  flowing  rapidly  into  the 
left  ventricle.  At  this  phase  of  diastole,  owing  to  the  stasis  in  the  pulmonary  veins,  the 
auricular  pressure  is  relatively  high.  It  is,  therefore,  not  surprising  that  the  stream  pass- 
ing through  the  narrowed  auricular  channel  under  about  the  same  pressure  should  give 
rise  to  a  rumble  similar  to  that  produced  later  in  diastole  when  the  same  stream  is  pro- 
pelled through  the  same  orifice  at  about  the  same  rate  by  the  force  of  the  auricular  con- 
traction.   Nor  is  it,  therefore,  surprising  that,  as  shown  by  Mackenzie,  the  early  diastolic 


MITRAL   STENOSIS.  351 

rumbles  produced  by  a  pressure  which  is  continually  diminishing  should  be  always 
decrescendo  in  character,  while  the  presystolic  rumbles  produced  by  the  rapidly 
increasing  auricular  contraction  should,  on  the  contrary,  be   crescendo. 

3.  A  blowing  diastolic  murmur  not  unlike  the  ordinary  mur- 
mur of  aortic  insufficiency  is  occasionally  heard  in  mitral  stenosis  (Graham 
Steell,  Huchard,  Cabot  and  Locke,  Bard).  This  murmur,  however,  never 
replaces  the  second  sound  as  does  the  aortic  murmur,  but  follows  it  after 
a  short  pause.  It  becomes  louder  and  lasts  longer  as  the  pulse-rate  dimin- 
ishes. The  murmur  is  intense  at  the  apex,  but  is  also  heard  above  and 
to  the  left  of  the  latter.  It  is  not  heard  over  the  aortic  area  nor  over  the 
sternum,  though  sometimes  heard  at  the  upper  left  sternal  margin.  Whether 
this  murmur  is  caused  by  a  secondary  functional  insufficiency  of  the  pul- 
monary valves,  due  to  dilatation  of  the  right  ventricle  (cf.  page  390),  or  is 
a  cardiopulmonary  murmur  (cf.  page  111)  induced  by  the  increased  activity 
of  the  right  ventricle,  is  still  unsettled.  It  is  probable  that  each  is  met  with 
in  some  cases. 

STAGES    OF    MITRAL    STENOSIS. 

It  is  difficult  to  divide  the  course  of  mitral  stenosis  into  well-defined 
stages.  From  a  physiological  and  diagnostic  stand-point  it  might  be  con- 
venient to  distinguish  four  stages, — which  differ  slightly  from  those  de- 
scribed by  Broadbent  (I.e.).  These  are  characterized  by  the  following 
phenomena: 

First  Stage.  —  Presystolic  rumble,  snapping  first  sound  and  second 
sound  are  well  heard  at  the  apex, — compensation  is  good, — the  left  auricle 
contracting  forcibly  as  shown  by  the  presystolic  rumble,  also  the  left  ven- 
tricle as  shown  by  well-marked  second  sound.  The  second  pulmonic  sound 
is  increased.  The  sounds  of  early  and  mid-diastole  may  or  may  not  be 
present.  Broadbent  says  of  this  stage,  "  I  have  never  known  serious  symp- 
toms to  arise  from  the  condition  of  the  heart,  and  I  have  seen  serious  ill- 
nesses of  different  kinds  passed  through  without  the  intervention  of  embar- 
rassment of  the  circulation." 

Second  Stage. — The  presystolic  rumble  and  first  sound  persist  and  the 
early  and  mid-diastolic  rumbles  may  be  present,  but  the  second  sound  at 
the  apex  has  completely  or  almost  completely  disappeared.  This  indicates 
that  the  force  of  the  left  ventricle  is  beginning  to  diminish  (Fig.  190,  III), 
but  the  left  auricle  is  still  contracting  forcibly.  At  this  stage  the  presystolic 
rumble  is  sometimes  mistaken  for  the  first  heart  sound  and  the  snapping 
first  sound  for  the  second,  so  that  if  there  is  a  systolic  murmur  present  a 
diagnosis  of  mitral  insufficiency  may  be  made,  and  a  less  severe  prognosis 
is  sometimes  given.  This  error  may  be  avoided  by  carefully  timing  the 
heart  sounds  by  palpation  or  by  noting  the  change  in  sounds  on  gradually 
passing  the  stethoscope  from  base  to  apex. 

Third  Stage. — The  presystolic  rumble  and  thrill  have  disappeared.  The 
snapping  first  sound  and  sounds  of  early  diastole  persist;  the  second  sound 
at  the  apex  may  or  may  not  be  heard.    Paralysis  of  the  left  auricle  has  set  in. 

Overlapping  of  Second  and  Third  Stages. — In  some  cases  this  occurs 
earlier  than  the  disappearance  of  the  first  sound  at  the  apex,  and  these 
two  stages  overlap  or  may  even  replace  one  another  chronologically. 


352  DISEASES   OF   THE    HEART    AND    AORTA. 

This  depends  upon  the  relative  strength  of  left  ventricle  and  left  auricle,  as  well  as 
upon  the  degree  to  which  the  mitral  orifice  is  narrowed;  for  a  comparatively  weak  left 
auricle  sometimes  fails  without  materially  affecting  the  cardiac  filling,  while,  on  the  other 
hand,  a  vigorously  beating  auricle  may  produce  a  loud  sound  while  forcing  a  small  amount 
of  blood  through  the  narrowed  orifice,  and  yet  the  amount  of  blood  thus  entering  the  left 
ventricle  may  be  too  small  to  maintain  the  arterial  blood-pressure  and  to  cause  a  distinct 
second  sound. 

Dyspncea,  haemoptysis,  and  the  usual  features  of  stasis  in  the  pulmo- 
nary circulation  occur  in  the  second  and  third  stages  of  the  disease. 

Fourth  Stage. — Broken  systemic  compensation,  venous  stasis,  oedema 
of  the  extremities,  enlargement  of  the  liver,  gastric  and  digestive  disturb- 
ances, ascites,  hydrothorax,  and  all  the  other  features  of  broken  compen- 
sation of  the  right  ventricle  set  in.  In  the  later  stages  there  are  well-marked 
signs  of  tricuspid  insufficiency,  positive  venous  pulse,  and  positive  pulsa- 
tion of  the  liver. 

PULSE. 

Exactly  as  in  mitral  insufficiency,  permanent  irregularity  of  the  pulse 
due  to  the  numerous  extrasystoles  may  occur  quite  early  in  cases  where 
both  the  presence  of  the  presystolic  rumble  and  the  venous  pulse  tracing 


CAR. 


JUG. 


— — __^ — __ 

— ^^ 

-— - 

— t-^         i- 

—- - — 

— 

—— — 

-■— — ■ 

c 

c 

c           c 

-j—^ — r 

-^       — r 

■  f" 

3.0 

5.0 

2.6 

4.0 

2.8 

4.0 

3.8 

1             a 

A 

\         ^ 

1                 a 

\         9^7 

I             1 

^    J\ 

-^IV 

-^ — ^    '^ 

W-*vc 

\J\ "      c 

c 

u- 

Va^L 

Fig.  200. — Permanent  arrhythmia  in  a  case  of  mitral  stenosis,  showing  persistence  of  the  auricular 
■contractions  (a  wave)  upon  the  venous  pulse.  The  right  auricle  (at  least)  is  still  contracting.  The  tracing 
shows  the  presence  of  persistent  auricular  extrasystoles. 

show  that  the  auricles  are  still  contracting  forcibly  (Fig.  200).  Owing  to 
the  greater  circulatory  disturbance  entailed  in  the  filling  of  the  left  ventricle, 
arrhythmia  causes  a  somewhat  greater  circulatory  disturbance  in  mitral 
stenosis  than  in  insufficiency,  although  in  neither  is  it  a  harbinger  of  immedi- 
ate danger  and  it  may  last  for  years.  The  pulse  is  usually  small  in  mitral 
stenosis,  owing  to  the  contracted  condition  of  the  radial  and  other  medium- 
sized  arteries. 

The  blood-pressure  is,  as  a  rule,  very  little  changed,  owing  to  the  com- 
pensatory changes  in  the  arterial  bed.  The  most  common  change  is  a 
diminution  in  pulse-pressure  due  to  a  rise  in  the  minimal  pressure  brought 
about  by  the  vasoconstriction.  A  large  pulse-pressure,  such  as  is  frequently 
seen  in  well-compensated  mitral  insufficiency,  is  not  common  in  mitral 
stenosis. 

DIAGNOSIS. 

In  the  absence  of  aortic  insufficiency  and  adherent  pericardium  the 
diagnosis  of  mitral  stenosis  is  comparatively  simple,  and  is  based  upon  the 
presence  of  the  presystolic  or  diastolic  rumble  or  thrill  at  the  apex,  together 
with  a  short  snapping  first  sound  in  this  region,  and  a  markedly  accentuated 
second  pulmonic  sound. 


MITRAL   STENOSIS.  353 

However,  it  sometimes  happens  that  these  signs  appear  only  occasion- 
ally while  the  patient  is  under  observation. 

Some  years  ago  the  writer  had  under  his  care  for  several  months  a  patient  with  per- 
nicious anaemia  in  whom  a  presystolic  murmur  was  heard  on  only  one  occasion,  though  the 
heart's  action  was  fairly  vigorous  and  regular.  A  gallop  rhythm  had  been  present  during 
her  entire  illness.    The  diagnosis  of  a  mild  grade  of  mitral  stenosis  was  verified  at  autopsy. 

Occasionally,  on  the  other  hand,  the  patient  is  seen  after  auricular 
paralysis  has  set  in  and  when  there  is  no  diastolic  rumble  present  whatever 
and  only  the  sounds  of  the  second  and  third  stages.  Such  cases  show  the 
need  of  frequent  auscultation  of  the  patient. 

Differentiation  between  Aortic  Insufficiency  and  Mitral  Stenosis. — In 
the  presence  of  aortic  insufficiency  it  must  be  remembered  that  the  presys- 
tolic and  diastolic  murmurs  described  by  Austin  Flint  may  closely  simulate 
those  arising  in  mitral  stenosis  (see  page  371).  In  aortic  insufficiency  the 
thrill  is  rarely  as  well  marked  as  in  mitral  stenosis,  and  the  first  sound  is 
rarely  sufficiently  short  and  snapping  to  be  mistaken  for  mitral  stenosis. 
The  two  conditions  were  found  together  in  4.2  per  cent,  of  the  1781  cases 
of  valvular  disease  at  the  Johns  Hopkins  Hospital, — i.e.,  in  about  one- 
seventh  of  all  the  cases  of  mitral  stenosis  and  one-tenth  of  all  the  cases  of 
aortic  insufficiency,  so  that  it  is  not  a  condition  of  extreme  rarity.  When, 
as  not  infrequently  happens,  the  mitral  stenosis  is  the  first  condition  present, 
there  is  no  difficulty,  as  the  late  diastolic  blow  of  mitral  stenosis  is  rare  and 
scarcely  ever  mistaken  for  aortic  insufficiency.  But  when  the  aortic  insuffi- 
ciency is  the  first  lesion  to  occur,  the  diagnosis  of  the  second  lesion  becomes 
much  more  difficult.  Occasionally  in  doubtful  cases  a  slight  exercise 
or  a  few  forced  expirations  with  glottis  closed  (Valsalva's  experiment)  will 
increase  the  work  of  the  left  auricle  and  cause  the  presystolic  thrill  and 
rumble  to  become  so  intense  that  the  presence  of  mitral  stenosis  is  unmis- 
takable. A  diagnosis  should  never  be  made  unless  the  heart  has  been 
examined  in  various  stages  of  its  activity.  In  spite  of  such  precautions 
errors  are  not  infrequent,  and  are  made  by  the  most  skilful  observers.  It 
must  be  frankly  confessed  that  there  are  many  cases  in  which  the  diagnosis 
cannot  be  made  with  any  degree  of  certainty. 

According  to  Phear,  adhesive  pericarditis  can  also  be  mistaken  for 
mitral  stenosis,  since  occasionally  a  presystolic  rumble  may  occur,  due  no 
doubt  to  the  stretching  of  the  fibrous  strands  under  the  influence  of  the 
auricular  contraction  of  the  ventricular  filling,  and  here  also  the  diagnosis 
of  two  coexistent  lesions  should  be  made  with  caution. 

Presystolic  Gallop  Rhythm. — Another  condition  which  on  rare  occa- 
sions may  be  confounded  with  mitral  stenosis  is  one  of  slight  cardiac  weak- 
ness in  which  there  is  a  presystolic  gallop  rhythm.  Under  these  circum- 
stances, as  Sewall  states,  the  ventricles  are  overfilled  with  blood  and  the 
auricle  encounters  some  difficulty  in  forcing  blood  into  them.  There  may 
even  in  some  cases  be  a  slight  functional  stenosis  like  that  discussed  on 
page  106.  Sewall  believes  that  under  these  conditions  the  contraction  of 
the  auricle  becomes  audible  and  may  even  be  mistaken  for  mitral  stenosis. 

Quite  recently  the  writer  has  had  under  his  care  in  the  Johns  Hopkins  Dispensary 
a  girl  of  13  years  who  presented  this  picture.    She  had  had  a  slight  attack  of  rheumatism 
and  tonsillitis  and  shortly  afterwards  began  to  .have  palpitation,  weakness,  nervousness, 
23 


354  disp:ases  of  the  heart  and  aorta. 

and  a  little  pain  in  the  precordium  and  around  the  lower  part  of  the  left  axilla.  On  exami- 
nation the  heart  was  not  enlarged,  but  the  shock  accompanying  the  first  sound  was  quite 
sharp  and  there  was  a  well-defined  impulse  which  began  with  vibrations  that  suggested  a 
presystolic  thrill.  These  were  somewhat  increased  on  exercise.  The  second  pulmonic 
was  not  abnormally  accentuated.  The  pulse-rate  was  120  and  regular.  There  was  no 
anaemia.  The  signs  were  not  quite  definite  enough  to  warrant  a  diagnosis  of  mitral  stenosis. 
The  patient  was  given  digitalis  for  a  few  days  and  this  was  followed  by  a  prolonged  treat- 
ment with  iron,  quinine,  and  strychnine.  She  improved  steadily,  an-l  for  several  week.< 
past  no  presystolic  sounds  or  impulse  can  be  elicited  even  by  quite  severe  exercise.  As  it 
seems  quite  vmlikely  that  an  auricular  paralysis  would  set  in  coincident  with  these  condi- 
tions of  improvement,  and  in  the  absence  of  any  arrhythmia,  it  seems  most  likely  that  this 
case  represented  one  of  very  loud  presystolic  gallop  rhythm,  and  that  no  organic  lesion 
is  present. 

Case  of  Mitral  Stenosis  vma  Ixsufficiency,  Axgix.v  Pectoris,  axd 
Pulmonary  Sclerosis. 

O.  A.  K.,  farmer,  aged  34,  was  admitted  to  the  Johns  Hopkins  Hospital,  June  2, 
1903,  complaining  of  heart  trouble  and  shortness  of  breath.  Family  history 
negative.  Patient  has  always  been  healthy  except  for  chorea  at  14  and  acute 
articular  rheumatism  at  18.  He  is  rather  subject  to  headaches.  Has  smoked  and 
drunk  in  excess,  but  for  the  past  few  years  does  so  in  great  moderation.  He  is  much  ex- 
posed to  the  weather. 

For  the  past  six  or  seven  years  he  has  been  short  of  breath  and  has  had 
pain  over  the  heart.  Six  months  before  admission  he  developed  ascending 
oedema,  which  disappeared  under  treatment,  but  his  breath  remained  short  and  the 
oedema  reappeared  within  a  couple  of  months.  During  the  past  month  he  has  had  spells 
of   dizziness   and  fainting  during  exertion  and  had  one  chill  followed  by  fever. 

On  examination  the  patient  is  seen  to  be  a  well-nourished  man  with  anxious  appear- 
ance and  flushed  face,  deeply  cyanotic.  He  is  quite  d  y  s  p  n  o  e  i  c  .  The  teeth  are 
bad;  the  pharynx  is  injected.  The  veins  of  the  neck  are  prominent,  but  do  not  pulsate. 
The  chest  is  full,  and  coarse  rales  are  everywhere  heard. 

Heart.  — The  apex  impulse  is  seen  in  the  6th  left  interspace  12  cm.  from 
the  midline.  Dulness  extends  upward  to  the  second  left  interspace  and  4  cm.  to  the  right 
of  the  sternum.  There  is  a  loud  systolic  mvirmur  heard  over  the  entire  heart 
and  left  axilla.  The  heart's  action  is  irregular  in  force  and  rhythm.  Pulse-rate  76.  The 
radial  is  somewhat  sclerotic.    Maximal  blood-pressure  130  mm.  Hg. 

His  liver  and  spleen  were  not  enlarged.    There  was  no  oedema  of  the  feet. 

He  was  kept  in  bed,  purged  freely,  given  tincture  of  digitalis 
(8  doses  of  1  c.c.  [tt\^xv]  each).  During  the  following  two  months  his  condition  im- 
proved markedly,  in  spite  of  the  occurrence  of  a  fibrinous  pleurisy.  His  dyspnoea 
diminished  and  he  felt  much  improved.  Coincident  with  this  improve- 
ment a  presystolic  rumble  and  thrill  gradually  appeared  and  a  s  n  a  ])  - 
ping  first  sound  preceded  the  systolic  murmur.  Three  months  after  admis- 
sion his  cyanosis  had  almost  entirely  disappeared.  The  heart  was  still  enlarged  (the  ape.x 
11  cm.  from  the  midline);  a  well-marked  presystolic  thiill  was  felt  and  a  presystolic  mur- 
mur was  heard  at  the  apex.  The  first  sound  was  snapping  and  was  accompanied  and 
followed  by  a  loud  blowing  systolic  murmur. 

The  blood-pressure  during  his  stay  in  the  hospital  ranged  between  12  0  and 
13  5  mm.   H  g  . 

After  leaving  the  hospital  at  this  time  the  patient  felt  well  for  about  six  weeks, 
during  which  period  he  could  even  run  for  a  car  without  distress.  Then  he  c  a  u  g  h  t  a 
cold  w^hich  persisted  for  four  months,  being  aggravated  by  exertion.  He  had  two  more 
fainting  spells  on  exertion.  Oedema  returned,  the  lower  extremities  and 
of  late  even  the  face  and  eyes  being  swollen.    Urine  less  frequent  than  normal. 

On  readmission  he  was  very  cyanotic  and  very  dyspnoeic. 
Moist  rales  were  heard  over  the  entire  chest.  The  apex  is  now  in  the  6th  left 
interspace  15.5  cm.  from  the  midline.  The  presystolic  rumble  and  sys- 
tolic murmur  are  well  heard,  as  at  the  last  discharge.  Red  blood-corpuscles  5,000.000; 
haemoglobin  105  per  cent.;  leucocytes  5500. 


MITRAL   STENOSIS.  355 

On  the  night  of  admission  the  patient  felt  badly  and  had  attacks  during 
which  he  felt  faint  and  "saw  stars."  Venesection  caused  much  releif 
in  the  symptoms  and  the  blood-pressure  rose  from  120  mm.  Hg  to  140  mm. 
The  patient's  condition  then  gradually  improved,  but  on  January  24  he  had  a  definite 
attack  of   precordial   pain   and   constriction   lasting  1-.3  minutes. 

Feb.  23.  Has  had  pain  in  head  and  the  left  side  of  the  face  due  to  a  beginning  otitis 
media. 

During  the  next  few  weeks  he  had  several  attacks  of  angina  pec- 
toris, the  pain  being  usually  most  marked  behind  the  lower  part  of  the  sternum.  In 
one  attack  it  radiated  to  the  left  shoulder  and  down  the  left  arm  to  the  hand  (left  ventric- 
vilar  pain). 

On  April  20  he  complained  of  pain  in  the  left  axilla  and  back,  com- 
ing  in   paroxys  ms   lasting   for    15-20   minutes    (left  auricular  pain) . 

May  6.  Sputum  bloody.  From  this  time  on  he  gradually  improved, 
cyanosis  and  dyspnoea  almost  disappeared,  and  he  was  discharged  in  August 
in  fair  condition.  From  that  time  until  his  readmission  in  November  he  suffered  from 
numerous  attacks  of  angina  pectoris,  beginning  in  the  left  hand  and 
passing  up  the  arm  to  the  shoulder  and  heart.  He  also  had  an  attack  of  rheu- 
matism and  severe  tonsillitis.  His  physical  condition  was  like  that  on  pre- 
vious admission,  but  the  anginal  attacks  were  more  frequent.  He  was  given  hypodermic 
injections,  sometimes  of  morphine,  sometimes  of  distilled  water,  to  relieve  them. 
His  condition  gradually  improved,  most  markedly  after  venesec- 
tion. Toward  the  end  of  his  stay,  while  up  and  about,  he  became  subject  to  sudden 
paroxysms  of  acute  dyspnoea  (respirations  130  per  minute),  with  small  moist  rales  filling 
the  lungs  (acute  pulmonary  oedema).  These  persisted  in  spite  of  repeated  rest  and  digitalis 
treatments.  He  was  discharged  on  July  11,  1905,  seven  months  after  admission,  ffidema 
and  dyspnoea  returned  within  ten  days,  and  he  was  soon  back  in  the  hospital  again.  Dur- 
ing this  admission  he  never  thoroughly  rallietl.  His  blood-pressure  remained 
low,  105  mm.  maximal  pressure  (as  compared  with  120-130  mm.  on  previous  ad- 
missions). The  pulse  was  irregular.  Rales  were  constantly  present  in  his  chest.  The 
liver  was  palpable.  A  slight  pleurisy  developed  on  October  13  and  he  died  on  Octo- 
ber 20. 

At  autopsy  the  mitral  orifice  was  foimd  to  have  the  form  of  a  small 
button -hole  barely  admitting  the  tip  of  the  little  finger  (about  5  mm.  in  diameter). 
The  left  auricle  was  dilated  and  hypertrophied.  The  left  ventricle 
was  not  dilated,  but  was  much  hypertrophied,  its  walls  being  15  mm.  thick.  The  right 
auricle  and  ventricle  were  much  dilated,  the  tricuspid  orifice  admitting  four  fingers 
(13-14  cm.  in  circumference).  The  coronary  arteries  were  patent  but  showed 
scattered  areas  of  sclerosis.  There  were  old  fibrous  patches  upon  the  pericardium. 
The  pulmonary  arteries  were  markedly  sclerotic  ;  the  sclerosis  extended 
into  their  smaller  branches.  The  aorta  and  peripheral  arteries  showed  less  sclerosis.  There 
were  also  chronic  passive  congestion  of  the  other  viscera,  anaemic  infarctions  of  the  spleen, 
hemorrhagic  infarction  of  the  lungs,  acute  bronchitis,  bronchopneumonia, 
acute  ulcerative  follicular  colitis,  old  tuberculous  foci  in  the  lymph-glands  and  lungs, 
chronic  adhesive  pleuritis,  and  adhesive  peritonitis. 


COMPLIC.\TIONS. 

As  seen  by  the  table  in  Fig.  179  mitral  stenosis  is  frequently  associated 
with  other  valvular  lesions.  Mitral  insufficiency,  present  in  one-half  of  the 
Johns  Hopkins  cases  and  in  75  per  cent,  of  Steell's  cases,  may  be  regarded 
as  an  essential  part  of  the  disease  rather  than  a  special  complication,  antl 
its  presence  does  not  shorten  the  average  length  of  life. 

The  association  of  aortic  disease,  and  indeed  of  any  additional  burden 
upon  the  circulation,  increases  the  gravity  of  the  condition. 

Tricuspid  stenosis  is  an  occasional  concomitant,  though  rarely  as  often 
found  as  by  Samways,  who  encountered  it  in  severe  grade  in  24  out  of  196 


356  DISEASES   OF   THE    HEART   AND    AORTA. 

autopsies  upon  cases  of  mitral  stenosis,  and  in  mild  grade  in  8  additional 
cases.  In  the  Johns  Hopkins  Hospital  it  was  found  clinically  7  times 
among  298  cases  of  mitral  stenosis. 

A  certain  degree  of  myocarditis  is  the  rule,  especially  in  cases  in  the 
third  and  fourth  decades. 

Acute  pericarditis  is  quite  common  in  the  youthful  rheumatic  cases, 
frequently  leaving  a  residual  adherent  pericardium,  a  lesion  which  aggra- 
vates the  condition  considerably  and  greatly  shortens  the  life  of  the  patient. 

One  of  the  most  important  and  dangerous  complications  arising  with 
mitral  stenosis  is  pregnancy  (see  Chapter  IX) . 

Thrombosis  in  the  Left  Auricle. — Another  not  uncommon  complica- 
tion of  mitral  stenosis,  more  than  any  other  valvular  lesion,  is  thrombosis 
within  the  left  auricle.  This  may  occur  even  while  the  auricle  is  still 
contracting  vigorously,  as  shown  by  the  presystolic  thrill  and  rumble. 
The  thrombus  may  remain  quiescent  in  the  tip  of  the  auricle  or  it  may 
obstruct  the  pulmonary  veins.  Sometimes  it  is  so  large  as  to  stop  up  the 
narrow  mitral  orifice  and  kill  the  patient.  More  frequently  it  is  small 
enough  to  pass  through,  and  if  carried  on  by  the  blood  current  gives  rise 
to  a  small  area  of  embolism. 

Embolism. — Embolism  of  the  middle  cerebral  artery  may  give  rise 
to  paralysis  or  aphasia.  Embolism  in  other  organs  gives  rise  to  correspond- 
ing signs  and  symptoms. 

Pulmonary  embolism  and  infarction  are  caused  by  thrombi  from  the 
right  auricle  and  ventricle;  and  hence  are  clue  to  secondary  stasis  in  the 
latter  and  not  primarily  to  the  mitral  stenosis.  However,  as  failure  of 
the  right  ventricle  is  particularly  common  in  mitral  stenosis,  pulmonary 
embolism  is  especially  frequent  in  this  disease. 

A  few  months  ago  a  patient  was  admitted  to  the  medical  service  of  the  Johns  Hopkins 
Hospital  with  gangrene  and  anaesthesia  of  both  lower  extremities,  due  to  plugging  of  the 
abdominal  aorta  by  such  an  embolus.  He  had  a  well-marked  mitral  stenosis,  with  purring 
presystolic  thrill  and  loud  presystolic  rumble,  showing  that  his  left  auricle  was  contracting 
vigorously.  Needless  to  say,  nothing  could  be  done  to  relieve  him,  and  he  died  within  a 
few  days. 

TREATMENT. 

The  treatment  of  mitral  stenosis  is  practically  the  same  as  that  of 
mitral  insufficiency,  except  that,  since  the  lesion  is  a  more  uniformly  pro- 
gressive one,  greater  care  must  be  exercised  in  the  general  hygiene,  espe- 
cially the  avoidance  of  infection  and  overstrain.  Digitalis  is  given  about 
as  in  mitral  insufficiency,  especially  when  the  left  ventricle  is  dilated. 

Amyl  nitrite  and  the  other  drugs  of  the  nitrite  group  may 
prove  of  value  when  there  is  a  broken  pulmonary  compensation.  Hydro- 
therapy and  gymnastics  may  be  used  after  the  pulmonary  compensation 
has  been  re-established,  but  must  be  administered  with  even  greater  care 
than  in  mitral  insufficiency,  for  acute  pulmonary  engorgement  and  pulmo- 
nary oedema  are  more  liable  to  set  in.  Since  it  is  particularly  important  to 
guard  against  dilatation  and  hypertrophy  of  the  right  ventricle,  vene- 
section should  be  performed  promptly  in  failure  of  the  latter,  especially 
if  there  are  signs  of  pulmonary  oedema,  unless  marked  anaemia  is  present. 


MITRAL  STENOSIS.  357 

Hypodermic  injections  of  atropine  0.5-1.0  mg.  (gr.  ttjj-gV)  maybe  given 
to  relieve  the  pulmonary  oedema  or  to  ward  it  off. 

Owing  to  the  role  of  anaemia  in  the  etiology  of  mitral  stenosis,  it  is 
especially  important  that  the  haemoglobin  be  kept  at  a  normal  level.  If 
anaemic,  the  patient  should  be  given  as  complete  rest  as  possible,  with 
maximal  amount  of  fresh  air  and  sunshine,  a  diet  especially  rich  in  eggs, 
on  account  of  the  lecithin,  and  iron  preparations,  especially  Blaud's  pills 
(0.3  Gm.,  gr.  v),  or  Vallet's  mass  (same  dose),  or  Ferrum  oxidatum  saccha- 
ratum  solubile  (one  teaspoonful  in  water),  should  be  administered  three 
times  a  day.  When  the  haemoglobin  is  near  60  per  cent,  or  the  progress 
slow,  arsenic  should  be  given  by  the  mouth,  especially  as  Fowler's  or  Dono- 
van's solution,  in  increasing  doses  until  1  c.c.  (15  minims)  is  reached.  Prof. 
J.  O.  Hirschfelder  obtains  excellent  results  by  the  hypodermic  injection 
of  1  per  cent,  sodium  arsenate  (1  c.c,  15  minims)  daily.  However,  this 
must  sometimes  be  discontinued  on  account  of  pain,  in  which  case  atoxyl 
may  be  substituted. 

W.  Arbuthnot  Lane  and  later  (1902)  Sir  Lauder  Brunton  suggested 
that  in  the  light  of  modern  surgical  technic  it  might  be  possible 
to  slit  the  narrowed  valve  with  a  fine  knife  and  thus 
remove  the  stenosis.  The  experiment  of  slitting  the  mitral  valve  has  been 
performed  by  Gushing  and  Branch  in  hearts  of  normal  dogs.  It  does  not 
present  extreme  difficulties,  but  the  recoveries  were  few,  in  spite  of  the 
fact  that  the  heart  muscle  of  these  dogs  was  in  good  condition.  Bernheim 
in  the  same  laboratory  arrived  at  similar  results.  Lauder  Brunton  had 
advocated  the  operation  only  for  cases  which  were  otherwise  doomed; 
and  it  is  evident  that  here  the  danger  from  a  weakened  myocardium  w^ould 
be  far  greater.  Moreover,  even  if  successful,  the  mechanical  effect  of  sud- 
denly converting  a  severe  mitral  stenosis  into  a  severe  mitral  insufficiency 
would  impose  an  intense  strain  upon  the  heart,  and  might,  even  in  that 
way,  do  more  harm  than  good. 

PROGNOSIS. 

In  spite  of  the  numerous  complications  and  the  progressive  character 
of  the  lesion,  the  average  duration  of  life  in  mitral  stenosis  is  not  extremely 
short,  being  33  years  for  males,  38  for  females.  This  is  due  to  the  large 
number  of  cases  in  which  the  process  is  dormant  or  progresses  very  slowly, 
and  indicates  in  the  individual  case  the  importance  of  avoiding  everything 
which  may  start  it  afresh,  particularly  infections  and  overstrain.  In  many 
cases  the  condition  then  remains  dormant  for  many  years,  the  patient  con- 
tinuing to  live  a  normal  if  somewhat  careful  life  without  further  trouble. 
Lenhartz  has  seen  cases  pass  through  seven  pregnancies  without  manifest- 
ing signs  of  cardiac  distress,  and  endurance  of  equal  magnitude  may  be 
met. with  in  men.  On  the  other  hand,  the  lesion  may  progress  rapidly  and 
death  may  occur  within  a  few  years.  In  the  more  severe  cases  it  may 
come  on  without  warning,  often  due  to  the  loosening  of  an  embolus  from 
the  left  auricle. 


358  DISEASES   OF   THE   HEART    AND    AORTA. 


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erzeugte  Mitralinsufficienz  und  ihren  Einfluss  auf  Kreislauf  und  Lunge,  Klin,  exper. 

Untere.  a.  d.  Lab.  S.  v.  Basch,  Berl.,  1891,  i,  144. 
Kornfeld,  S.:  Exf>erimentelle  Beitrag  zur  Lehre  vom  Venendruck  bei  Fehlern  des  linken 

Herzen,  ibid.,  1892,  ii,  126. 
Gerhardt,  D.:  Ueber  die  Compensation  von  Mitralfehlern,  Arch.  f.  exper.  Pathol,  u.  Phar- 

makol.,  Leipz,  1901,  xlv,  186. 
MacCallum,  W.  G.,  and  McClure,  R.:  On  the  Mechanical  Effects  of  Mitral  Stenosis  and 

Insufficiency,  Ti'.  Ass.  Am.  Phys.,  Phila.,   1906,  xxi,  5;    also  Bull.  Johns  Hopkins 

Hosp.,  Baltimore,  1906,  xvii,  260. 
Hirschfelder,  A.  D.:  The  Volume  Curve  of  the  Ventricles  in  Experimental  Mitral  Stenosis 

and  its  Relation  to  Physical  Signs,  Bull.  Johns  Hopkins  Hospital.  Baltimore,  1908,  xix. 
Midler,   G.:  Ungewohnliche  Dilatation   des   Herzens   imd   Ausfall   der  Vorhofsf unction, 

Ztchsr.  f.  klin.  Med.,  Berl.,  1905,  Ivi,  520. 
Harris,  Th.     Quoted  on  p.  340. 
Petit,  A.:  Retr^cissement  mitrale,  Traits  de  Med.  (Charcot,  Bouchard,  Brissand),  Paris, 

1893,  V,  247. 
Corvisart,  J.  N. :  An  Essav  on  the  Organic  Diseases  of  the  Heart,  etc.,  translated  bv  Jacob 

Gates,  Phila.,  1812. 
Gendrin  and  Fauvel:  Arch,  de  M^d.,  Paris,  1843,  S6r.  iv,  i,  1.     Quoted  from  Gairdner. 
Gairdner,  W.  T. :  A  Short  Account  of  Cardiac  Murmurs,  Edinb.  M.  J.,  1861,  vii,  428;  also 

Clinical  Medicine,  1862. 
Mackenzie,  James:  The  Study  of  the  Pulse  and  Movements  of  the  Heart,  Lond.,  1903. 

The  Extrasystole,  etc.,  I,  Quart.  J.  M.,  Lond.,  1907,  i,  131,  481. 
Minkowski,  O.:  Demonstration  eines  Herzens  mit  ungewohnlich  starker  Dilatation  der 

Vorhofe,  Mimchen.  med.  Wchnschr.,  1904,  li,  182. 
Hofbauer:  Rekurrenslahmung   bei    Mitralstenose,    Wien.    klin.    Wchnschr.,    1902.      Also 

Alexander:  Berl.   klin.   Wchnschr.,    1904;    and   Frischauer:  Wien.   klin.    Wchnschr., 

1905.     Quoted  from  Thorel,  C:  Pathologic  der  Kreislauforgane,  Lubarsch-Ostertag's 

Ergebnisse  der  Path.,  Wiesb.,  1907,  ii,  iite  Abth.,  386. 
Osier,  W. :  De  la  paralysie  du  nerf  recurrent  gauche  dans  les  affections  mitrales,  Arch,  des 

malad.  d.  coeur.  Par.,  1909,  ii,  73.    Reviewed  in  an  editorial,  J.  Am.  M.  Ass.,  Chicago, 

1909,  liii,  35. 

Einthoven,  W.,  with  the  assistance  of  Flohil  and  Battaerd:  Die  Registrirung  der  mensch- 
lichen  Herztone  niittelst  des  Saitengalvanometers,  Arch.  f.  d.  ges.  Physiol.,  Bonn, 
1907,  cxvii.  461. 

Brockbank,  E.  M.:  The  Murmurs  of  Mitral  Disease,  Edinb.  and  Lond.,  1899. 

Fenwick,  W.  S.,  and  Overend,  W.:  The  Production  of  the  First  Cardiac  Sound  in  Mitral 
Stenosis,  Am.  J.  M.  Sci.,  Phila.,  1893,  ex,  123. 


MITRAL   STENOSIS.  359 

Hiivcraft,  J.  B.:  The  Cause  of  the  First  Sound  of  the  Heart,  J.  Physiol.,  Camb.,  1890,  xi, 
'486. 

Broadbent,  W.  H.,  and  J.  F.  H.:  Heart  Disease  and  Aneurism,  N.  Y.,  1906. 

Acland.     Quoted  from  Fenwick  and  Overend. 

Steell,  G.:  The  Auscultatory  Signs  of  Mitral  Obstruction  and  Regurgitation,  Med.  Chron., 
Manchester,  1888,  viii,  89.  The  Diagnosis  of  Mitral  Regurgitation  through  a  Con- 
stricted Orifice,  ibid.,  1891-2,  .xv,  361.  The  Conduction  of  the  Murmur  of  Mitral 
Regurgitation,  ibid.,  1892,  xvi,  116.  The  Distinction  between  Mitral  Stenosis  and 
Muscle-failure  in  Certain  Heart  Cases,  ibid.,  1892-3,  xvii,  24.  The  Auscultatory  Signs 
of  Mitral  Stenosis;  a  Statistical  Inquiry,  ibid.,  1895,  N.  S.  iii,  409.  Case  of  Mitral 
Stenosis  presenting  a  Widely  Distributed  To-and-fro  Murmur  Resembling  that  of 
Aortic  Incompetence,  ibid.,  1896-7,  N.  S.  vi,  174.  Mitral  Stenosis,  Internal.  Clin., 
Phila.,  1898,  s.  viii,  iii,  1411. 

Huchard:  I.e.,  p.  569. 

Cabot,  R.  C,  and  Locke,  E.  A. :  On  the  Occurrence  of  Diastolic  Murmurs  without  Lesions 
of  the  Aortic  or  Pulmonary  Valves,  Bull.  Johns  Hopkins  Hosp.,  Baltimore,  1903,  xiv, 
115. 

Bard,  L.:  Die  Phvsikalische  Zeichen  der  Mitralstenose,  Samml.  kiln.  Vort.,  Leipz.,  No.  45, 
Inn.  Med.  No.  137,  1907. 

FHnt,  A.:  The  Mitral  Cardiac  Murmurs,  Am.  J.  M.  Sc,  1886,  xci,  27. 

Phear,  A.  G.:  On  Presystohc  Apex  Murmur  without  Mitral  Stenosis,  Lancet,  Lond.,  1895, 
ii,  718. 

Weber  and  Deguy:  Du  role  des  haemorrhagies  intracardiaques  dans  le  retrecissement 
mitral.  Arch,  de  Med.  Exper.,  Par.,  1897,  and  Presse  m^d.,  Par.,  1898. 

Sewall,  H.:  A  Common  Modification  of  the  First  Heart  Sound,  etc.,  Trans.  Ass.  Am.  Phys., 
Phila.,  1909,  and  Am.  J.  M.  Sc,  1909. 

Brunton,  T.  Lauder:  Preliminary  Note  on  the  Possibility  of  Treating  Mitral  Stenosis  by 
Surgical  Methods,  Lancet,  Lond.,  1902,  i,  352.  Discussed  by  Shaw,  L.  E.,  ibid.,  1902, 
i,  619. 

Cushing,  H.  W.,  and  Branch,  J.  R.  B.:  Experimental  and  Clinical  Notes  on  Chronic  Val- 
vular Lesions  in  the  Dog  and  their  Possible  Relation  to  a  Future  Surgery  of  the  Cardiac 
Valves,  J.  Med.  Research,  1908,  xii. 

Bernheim,  B.  M.:  Experimental  Surgery  of  the  Mitral  Valve,  Johns  Hopkins  Hospital 
Bull.,  Baltimore,  1909,  xx,  107. 


IV. 

AORTIC  INSUFFICIENCY. 


HISTORICAL. 

Our  knowledge  concerning  lesions  of  the  aortic  valves  producing  leak- 
age at  that  orifice  (aortic  insufficiency,  aortic  regurgitation,  aortic  incom- 
petency) dates  from  1705,  when  the 
English  anatomist  Cowper  first  de- 
scribed the  occurrence  of  stiffening 
and  thickening  of  the  valves  so  that 
they  "did  not  apply  adequately  to 
each  other,  whence  it  happened  some- 
times that  the  blood  in  the  great 
artery  would  recoil  and  interrupt  the 
heart  in  its  systole."  Shortly  after 
this,  and  quite  independently  of  Cow- 
per, Vieussens  (1715)  described  two 
similar  cases,  noting  also  the  presence 
of  a  very ,  full  quick  pulse,  like  the 
rebound  of  a  tightly-stretched  cord, 
associated  with  palpitation  of  the 
heart  so  severe  that  it  prevented  lying 
down.  Morgagni  also  described  sev- 
eral cases,  in  one  of  which  he  recog- 
nized both  aortic  insufficiency  and 
aortic  stenosis.  Hodgkin  in  1829  de- 
scribed a  number  of  cases,  and  also 
noted  for  the  first  time  the  diastolic 
murmur,  but  did  not  recognize  any 
diagnostic  features;  so  that  the  clear 
clinical  picture  of  aortic  insufficiency  may  be  said  to  date  from  the 
publication   of   Dominic   Corrigan  in   1832. 


L 

Ml 

H&l 

^\ 

\%ffej 

J 

w 

Fig.  201.  —  Specimen  showing  vegetations 
upon  the  aortic  valves.  The  arrow  points  to  the 
vegetation. 


PATHOLOGICAL    ANATOMY. 

Modern  classifications  of  aortic  insufficiency  differ  little  from  that  of 
Corrigan,  and  we  distinguish,  as  he  did — 

1.  Organic  forms  of  aortic  insufficiency  due  to  pathological  changes  in  the  valves. 

2.  Functional  or  relative  aortic  insufficiency  due  to  dilatation  of  the  mouth  of  the 

aorta  (Fig.  202,  D). 

The  organic  forms  of  aortic  insufficiency  may  be  of  three  types: 

1.  Endocarditic,  due  to  the  occurrence  of  inflammatory  changes  upon  the  valves, 
usually  vegetations,  occasionally  to  calcified  atheromatous  plaques  (Fig.  202,  A). 
360 


AORTIC   INSUFFICIENCY. 


361 


2.  Rupture  of  the  valves,  sometimes  from  mechanical  strain,  sometimes  from  ulcera- 

tion (Fig.  202,  B). 

3.  Sclerotic  shrivelling  of  the  cusps,  usually  associated  with  arteriosclerosis  (Fia:, 

202,  C). 

1.  The  pathology  of  the  endocarditic  lesions  has  been  sufficiently  dis- 
cussed in  a  preceding  chapter  (page  299) ,  since  they  represent  quite  typi- 
cal vegetations.  This  form  of  lesion  results  from  the  usual  causes  of 
endocarditis,  especially  rheumatism,  scarlet  fever,  pneumonia,  as  well  as 
gonorrhoeal,  puerperal,  septicsemic,  and  other  acute  infections  (see  page 
301).  It  is  the  most  common  form  in  persons  below  thirty-five,,  whereas 
the  sclerotic  is  more  common  in  later  life. 

2.  Rupture  of  the  valves  is  one  of  the  less  frequent  but  by  no  means 
rare  occurrences,  and  usually  takes  place  suddenly  during  a  period  of  great 
muscular  strain,  such  as  wrestling,  lifting  a  heavy  weight,  drawing  a  heavy 
burden,  or  even  during  a  bicycle  race  (Huchard),  or  else  after  severe  blows 
upon  the  chest  (Osier).  Under  these  circumstances,  as  has  been  seen, 
the  blood-pressure  may  suddenly  rise  to  a  tremendous  height  (see  page  132), 


Fig.  202. — Schematic,  showing  the  various  forms  of  lesion  producing  aortic  insufficiency.     A.  Vegetation. 
B.  Perforation.     C.  Artferiosclerotic  shrinking.     D.  Dilatation  of  the  aorta. 


and  the  blood  stream  tears  its  way  through  the  valve  at  the  weakest  point — 
usually  near  the  base  of  the  sinus  of  Valsalva.  The  ruptured  valve  may 
have  an  apparently  normal  structure,  but  probably  contains  minute  areas 
of  degeneration,  since  it  is  impossible  to  rupture  a  normal  valve  experi- 
mentally by  subjecting  it  to  the  highest  pressures  that  are  ever  reached  in 
the  animal  body.  In  many  cases  the  ruptured  valves  show  arteriosclerotic 
changes  which  have  tended  to  weaken  the  tissue.  Where  endocarditic 
changes  are  already  present,  rupture  or  perforation  of  the  valve  takes  place 
spontaneously  and  at  ordinary  or  even  lowered  blood-pressures. 

3.  The  sclerotic  form  of  the  lesion  is  not  only  the  most  common, 
but  produces  the  lesions  which  are  most  uniformly  severe  and  progressive, 
since  it  usually  occurs  in  later  life  and  is  associated  with  general  arterio- 
sclerosis (Fig.  202,  C) .  The  lesion  is  in  every  way  similar  to  the  sclerotic  proc- 
ess elsewhere  in  the  aorta,  and  may  assume  any  of  the  types  which  occur 
in  general  arteriosclerosis — thickening  with  contraction,  calcification,  aneu- 
rismal  dilatation,  perforation.  In  any  individual  case  the  symptoms 
depend  upon  the  size  of  the  leak  as  well  as  upon  the  state  of  the  peripheral 
vessels  and  the  heart. 

The  etiological  factors  bringing  about  this  lesion  are  the  same  as  those 
given  for  general  arteriosclerosis  (see  page  254),  infections,  alcohol,  tobacco, 
lead  poisoning,  nephritis,  hard  work.  Osier  (1.  c.)  especially  calls  atten- 
tion to  the  fact  that  syphilis  is  one  of  the  most  frequent  causes  of  sclerosis 


362  DISEASES   OP^   THE    HEART    AND    AORTA. 

about  the  root  of  the  aorta  in  men  under  thirty-five,  and  that  the  lesions 
commonly  involve  both  the  aortic  valves  and  the  mouths  of  the  coronary 
arteries.  He  considers  this  factor  next  to  endocarditis  in  order  of  impor- 
tance as  a  cause  of  aortic  insufficiency  in  young  men.  Collins  and  Sachs 
and  Longcope  have  recently  obtained  a  positive  Wassermann  reaction  in 
about  half  the  cases  of  aortic  insufficiency  in  which  there  had  been  no  out- 
spoken rheumatism. 

Sex. — In  women  aortic  insufficiency  is  far  less  frequent  than  in  men, 
constituting  8.4  per  cent,  of  all  heart  lesions  in  the  former  as  compared  with 
"28.5  per  cent,  in  the  latter  (Gillespie). 

Moreover,  as  shown  by  Romberg  and  Hasenfeld,  the  presence  of  aortic 
insufficiency  from  causes  other  than  sclerosis  in  itself  leads  to  the  produc- 
tion of  general  arteriosclerosis,  and  hence  the  presence  of  any  other  form 
of  the  lesion  predisposes  to  the  superposition  of  sclerosis. 

Functional  Aortic  Insufficiency. — The  existence  of  leaks  at  a  dilated  aortic  orifice 
was  already  suspected  by  Corrigan,  especially  when  there  was  an  aneurism  ne:xr  the  base  of 
the  ascending  arch.  This  has  been  verified  by  subsequent  observers  and  a  diffusely  dilated 
aorta  with  insufficiency  of  the  valves  is  not  a  rare  finding.  As  regards  the  presence  of  tran- 
sitory leaks  from  dilatation  Gibson  has  also  shown  experimentally  that  such  a  dilata- 
tion may  occur  as  a  result  of  too  high  pressure  in  the  excised  heart,  and  Stewart  claims  to 
have  produced  it  by'  cutting  the  aortic  ring  muscle.  But  since  transitory  aortic  insufficiency 
does  not  often  accompany  the  high  blood-pressures  of  uraemia,  meningitis,  and  brain  tumor, 
it  is  probable  that  this  factor  plays  little  role  clinically.  The  cases  of  supposed  functional 
aortic  insufficiency  are  rare,  but  Anders  has  reported  a  considerable  number.  In  some  at 
least  it  is  possible  that  the  phenomena  (diastolic  murmur,  collapsing  pulse,  etc.)  are  due 
to  other  causes,  especially  functional  pulmonary  insufficiency.  Cardiopulmonary 
murmurs,  like  those  described  by  Potain,  must  also  be  excluded.  However,  the  possi- 
bility of  functional  aortic  insufficiency  must  be  borne  in  mind  by  the  clinician;  but  it  can 
rarely  be  verified,  and  the  clinical  diagnosis  is,  at  best,  hazardous. 


Fig.  203. — Effect  of  aortic  insufficiency  in  the  mechanical  model.  (After  Marey.)  The  horizontal 
Ime  shows  the  point  of  production  of  aortic  insufficiency.  P.V.,  intraventricular  pressure;  PR.  arterial 
pressure;  O,  auricular  systole.  The  diastolic  pressure  in  the  ventricle  after  aortic  insufficiency  is  consid- 
erably higher  than  in  the  normal  condition  and  approximates  the  diastolic  pressure  in  the  aorta.  The 
wavelet  o',  due  to  contraction  of  the  auricle,  is  less  marked. 

P.\THOLOGIC.\L    PHYSIOLOGY. 

The  mechanical  effects  of  aortic  insufficiency  upon  the  circulation  were 
first  studied  experimentally  in  horses  and  dogs,  as  well  as  on  the  mechanical 
model,  by  Marey  and  Chauveau. 


AOJITIC   IXSUFFICIKXCY 


363 


They  produced  the  lesion  by  pushing  a  probe  down  one  carotid  artery  and  through  a 
cusp  of  the  aortic  vahe,  while  they  registered  the  pulsation  in  the  other  carotid  by  means 
•of  a  cannula.  They  were  thus  able  to  reproduce  the  phenomena  observed  clinically, 
especially  the  occurrence  of  the  nuirmurs,  the  violent  beating  of  the  heart  and  arteries, 
and  the  large  collapsing  pulse  which  had  been  described  by  Corrigan.  They  were  also 
able  to  rei)roduce  these  phenomena  in  a  mechanical  model  of  the  circulatory  system. 

The  experiments  of  Marey  and  Chauveau  on  animals  have  been  repeated  and  con- 
firmed by  Cohnheim,  Rosenbach,  de  Jaager,  Kornfeld,  Romberg  and  Hasenfeld,  and  those 
upon  the  model  by  Moritz.  The  subject  was  again  investigated  under  the  writer's  direction 
by  Dr.  H.  A.  Stewart  in  the  Johns  Hopkins  Medical  Clinic.  The  method  employed  by 
-Stewart  differed  from  that  of  previous  observers  in  the  fact  that  he  recorded  simultaneously 
the  volume  of  the  ventricles,  the  maximal  and  minimal  blood-pressures,  and  the  pulse- 
curve  from  the  carotid  artery.  He  found  in  animals,  as  had  been  shown  by  Marey  upon 
the  mechanical  model,  that  the  production  of   aortic    insufficiencv    is    at 


NORMAL 


II 

COMPENSATED 

LOW  PERIPHERAL 

RESISTANCE 


III  I 

I 

COMPENSATED 

HIGH  PERIPHERAL 

RESISTANCE 


IV 

BROKEN 

PULMONARY 

COMPENSATION 


Fig.  204. — Diagram  of  the  circulation  in  aortic  insufficiency.  The  vertical  black  bars  represent  the 
"volume  of  tlie  left  ventricle,  the  shaded  portions  representing  the  residual  blood,  the  portions  indicated  by 
the  white  arrows  showing  the  amount  of  blo<xl  regurgitating,  the  solid  black  indicating  the  systolic  output. 
The  black  arrows  indicate  the  change  in  condition  or  pressure  that  has  taken  place.  MAX,  MIN,  max- 
imal and  minimal  bloofi-pres.sures.  The  white  curve  indicates  the  absolute  .sphygmogram  corresponding. 
AO,  PA,  RA,  LA  as  in  previous  diagrams. 


once  folio  ^\ed  by  a  great  fall  in  i>ressure  during  diastole, 
which  is,  at  least  in  part,  due  to  the  regurgitation  into  the  ventricle.  This  great  fall  in 
diastolic  pressure  is  the  most  characteristic  featiu'e  of  aortic  insufficiency. 

The  actual  amount  of  blood  regurgitating,  both  in  animals  (Stewart) 
and  in  model  experiments  (Moritz),  is  usually  not  more  than  o  n  o  -  t  e  n  t  li  of  the 
total   forced   out    at   each   systole. 

As  in  the  case  of  ^ovr  through  any  orifice,  the  factors  influencing  this 
regurgitation  are:  (1)  the  size  of  the  hole  in  or  between  the  valves;  (2) 
the  head  of  pressure  in  the  aorta;  (3)  the  length  of  time  during  which 
leakage  occurs. 

Cardiac  Tonicity. — The  experiments  pei'formed  by  Stewart  and  the 
writer  indicate  that  the  chief  factor  antagonizing  the  reflux  is  the  elasticity 
■of  the  heart  muscle,  or  the  cardiac  tonicity. 

It  is  evident  that,  with  a  given  lesion  and  a  constant  heart  rate,  the 
factor  affecting  the  regurgitation  is,  therefore,  the  antagonism  between  the 
height  of  blood-pressure  during  diastole,  on  the  one  hand,  and  the  cardiac 
tonicity,  on  the  other.     However,  the  pres.sure  within  the  ventricle  is  not 


364 


DISEASES   OF   THE   HEART   AND   AORTA. 


constant  throughout  diastole,  but  is  continually  increasing;  while  the  pres- 
sure in  the  aorta  is  continually  decreasing,  and  the  reflux  will  cease  alto- 
gether at  the  instant  when  pressure  within  the  ventricle  +  cardiac  tonicity 
=  pressure  within  the  aorta.  Consequently,  the  lower  the  pressure  in  the 
aorta  (diastolic  pressure)  or  the  higher  the  cardiac  tonicity,  the  earlier  this 
will  occur  and  the  less  will  be  the  amount  of  blood  regurgitating. 


AORTIC  PRESSURE 
INTRAVENTRICULAR  PRESSURE 


AMOUNT  OF  BLOOD 
REGURGITATING 


Fig.  205. — Diagram  showing  how  the  high  cardiac  tonicity  (7*  +)  hastens  the  equilibrium  between  aortic 
pressure,  intraventricular  pressure,  and  tonicity,  and  thus  diminishes  the  amount  of  blood  regurgitating. 

It  was  found,  however,  that  whenever  this  occurred  the  hearts 
dilated  and  the  animals  died.  Those  animals  which  survived  the  shock  of 
the  operation  were  able  to  increase  their  systolic  output  by  the  amount 
regurgitated,  and  thus  in  spite  of  the  lesion  to  keep  the  maximal  pressure 
at  the  same  height  as  before.  In  these  animals  positive  intraventricular 
pressure  during  diastole  acts  as  a  load  to  the  heart  muscle,  which  responds 


wmmi\A 


T  + 


NORMAL 


DILATATION 


DIMINUTION    IN   VOLUME 


Fig.  206. — Eflfect  of  rupturing  an  aortic  valve  in  a  dog,  showing  a  transitory  dilatation  followed  by  a 
permanent  diminution  in  size.  (After  Stewart.)  C^ ft.,  carotid;  VOL.,  volume  of  the  ventricles.  Down- 
strokes  represent  systole,  upstrokes  diastole.  The  maximal  blood -pressure  remains  unchanged  (122  mm. 
Hg),  the  minimal  pressure  falls  from  90  to  45  mm.  Systolic  output  is  somewhat  increased,  a-b  repre- 
sents the  tonicity  of  the  ventricles  before  producing  the  lesion;  c-d  represents  tonicity  after  the  lesion.  A 
represents  the  point  at  which  the  aortic  valve  was  ruptured. 

by  increased  tonicity,  and  fills  somewhat  less  completely  than  it  otherwise 
would;  so  that  the  total  volume  of  the  ventricles  after  aortic  insufficiency, 
just  as  after  any  other  strain,  may  be  smaller  than  before  it.  In  these  hearts 
total  volume  is  decreased,  systolic  output  increased,  and  residual  blood 
greatly  decreased. 

Romberg  and  Hasenfeld  (1.  c.)  have  denied  that  this  increased  tonicity  is  always 
beneficial,  claiming  that  by  inhibiting  the  inflow  from  the  auricle  it  impedes  the  circulation. 
However,  Komfeld  found  that  the  pressure  in  the  left  auricle  is  not  affected  by  experi- 


AORTIC   INSUFFICIENCY.  .  365 

mental  aortic  insufficiency  as  long  as  the  strength  of  the  left  ventricle  remains  unimpaired. 
As  the  influences  which  maintain  tonicity  are  in  almost  every  instance  the  same  as  those 
which  increase  the  strength  and  volume  of  the  systole,  it  is  probable  that  Romberg  and 
Hasenfeld  are  in  error. 

As  regards  the  role  played  by  tonicity  in  aortic  insufficiency  two  views 
are  held: 

1.  Romberg  and  Hasenfeld  claim  that  an  increased  tonicity  hindering 
the  influx  of  blood  from  the  auricle  is  distinctly  harmful. 

2.  Stewart  and  the  writer  have  shown  that  the  most  dangerous  event 
in  experimental  aortic  insufficiency  is  overdilation,  and  this  is  antagonized 
by  increase  in  tonicity.  Moreover,  Cloetta  has  found  that  the  hearts  of 
rabbits  with  experimental  aortic  insufficiency  which  had  been  treated  with 
digitalis  were  less  dilated  and  were  much  stronger  than  those  of  normal 
rabbits.  Almost  all  the  influences  which  bring  about  increased  systolic 
output  are  the  same  as  produce  increase  in  tonicity.  Fear  of  evil  results 
from  this  cause  seems,  therefore,  quite  unwarranted. 

Blood=pressure. — As  regards  blood-pressure,  it  was  found  that  when 
the  peripheral  resistance  was  increased,  as  by  clamping  the  thoracic  aorta, 
the  force  of  the  heart-beat  increased  correspondingly,  and  both  maximal 
and  minimal  (systolic  and  diastolic)  pressures  increased  about  equally 
and  pulse-pressure  remained  high.  With  the  increase  in  diastolic  pressure 
upon  clamping,  the  regurgitation  through  the  orifice  increased  (Fig.  214), 
and,  as  systolic  output  changed  no  further,  the  heart  dilated  considerably, 
showing  that  high  peripheral  pressure  represents  the  condition  which 
produces  the  greatest  embarrassment  of  the  circulation.  With  the  increase 
in  peripheral  pressure,  however,  the  form  of  the  pulse  curve  changed 
from  collapsing  to  flat-topped  and  anacrotic,  a  fact  which  will  be  referred 
to  later. 

Rate. — Corrigan  thought  that  if  the  heart  were  slowed  and  diastole 
were  prolonged  the  heart  would  undergo  great  dilatation,  but  in  the  experi- 
ments performed  by  Stewart  and  the  wriler  it  can  be  seen  that  this  dilata- 
tion soon  reaches  its  limit,  and  the  volume  of  the  ventricles  need  not  exceed 
the  normal  volume  for  the  same  rate  (Fig.  206).  This  is  due  to  the  fact 
that,  as  the  aortic  pressure  falls  during  a  prolonged  diastole,  it  approaches 
the  intraventricular  pressure,  and  the  above-mentioned  equilibrium  is 
soon  reached. 

As  a  result  of  experiments  upon  animals,  it  would  appear,  therefore, 
that  the  conditions  most  favorable  to  the  heart  are  low  peripheral  resist- 
ance and  moderately  high  tonicity;  and,  as  will  appear  later,  therapy  should 
be  directed  toward  this  end. 

Pulmonary  Circulation. — As  stated  above,  Kornfeld's  experiments 
show  that  the  aortic  lesion  has  no  effect  upon  the  pulmonary  circulation  as 
long  as  the  left  ventricle  is  acting  powerfully.  When  the  left  ventricle 
begins  to  fail,  pulmonary  stasis  and  rise  in  auricular  pressure  occur  (Korn- 
feld),  which,  as  Stewart  and  the  writer  have  found,  are  frequently  associated 
with  the  occurrence  of  a  functional  mitral  insufficiency.  Pulmonary  stasis 
in  aortic  insufficiency  is,  therefore,  a  secondary  phenomenon  dependent 
upon  failure  of  the  left  ventricle.  The  clinical  importance  of  this  fact  will 
be  referred  to  subsequently. 


366  DISEASES   OF   THE    HEART    AND    AORTA. 

Hypertrophy. — As  a  result  of  the  increased  strain  upon  the  left  ventricle., 
the  walls  of  this  chamber  undergo  great  hypertrophy.  The  cavity  of  the  left 
ventricle,  owing  to  the  regurgitation  during  diastole,  is  often  much  dilated, 
especially  in  the  infrapapillary  or  aortic  portion  of  the  chamber. 

The  left  auricle,  on  the  other  hand,  is  rarely  hypertrophied.  The  right 
ventricle,  however,  usually  shows  some  hypertrophy,  resulting  either  from 
slight  increase  in  pulmonary  pressure  or  from  continuity  of  the  fibres  with 
those  of  the  left  ventricle. 

SYMPTOMS. 

The  .symptomatology  of  aortic  insufficiency  differs  considerably  from 
that  of  the  mitral  lesions.  When  the  lesion  is  well  compensated  and  no 
pulmonary  stasis  occurs,  dyspnoea  may  not  appear  for  years,  and  in  the 
meantime  the  patient  may  enjoy  excellent  health.  On  the  other  hand, 
he  may  also  be  considerably  annoyed  by  the  throbbing  of  his  arteries, 
headache,  roaring  in  the  ears,  by  loss  of  memory,  by  periods  of  depression 
often  alternating  with  periods  of  great  exhilaration,  by  the  appearance  of 
motes  or  muscse  volitantes  before  the  eyes. 

Hallucinations  of  sight,  especially  that  of  the  veiled  gray  figure,  of  hearing 
(rhythmic  knocking  or  bell-tolling),  and  of  smell  are  relatively  common  in  aortic  disease, 
and  are  usually  associated  with  pain  in  the  precordium  or  down  the  arms  and  tenderness 
over  the  upper  left  chest  (Head).  Head  states  that  these  always  disappear 
when   mitral   insufficiency   sets  in. 

There  are  often  pains  over  the  heart,  especially  over  the  base,  and 
down  the  left  arm,  and  typical  attacks  of  definite  angina  pectoris.  These 
symptoms  are  especially  common  in  the  sclerotic  forms,  in  the  later  stages 
of  the  disease,  but  may  occur  even  when  the  coronary  arteries  are  unaffected. 
After  the  break  in  compensation,  dyspncea  is  usually  intense,  and  the  patient 
is  compelled  to  sit  up  in  bed,  not  only  on  account  of  shortness  of  breath 
but  also  on  account  of  extreme  palpitation. 

Cheyne-Stokes  respiration  (of  the  cardiac  type)  is  some- 
what more  common  in  aortic  insufficiency  than  in  other  forms  of  cardiac 
disease.  Undoubtedly  this  is  due  to  some  disturbance  in  the  medullary 
circulation,  but  the  exact  explanation  is  still  uncertain. 

Sudden  agonizing  attacks  of  cardiac  asthma  are  very  fre- 
quent, accompanied  by  intense  orthopncea,  in  which  the  patient  gasps  for 
breath  for  several  minutes  or  even  half  an  hour.  No  doubt  they  are  asso- 
ciated with  sudden  overfilling  of  the  left  ventricle,  secondary  functional 
mitral  insufficiency,  and  pulmonary  stasis.  Sudden  death  may  occur  dur- 
ing such  attacks,  and  is  indeed  more  common  in  aortic  insufficiency  than 
in  other  forms  of  valvular  disease.  Both  the  maximal  and  the  minimal 
pressures  may  be  high  up  to  the  instant  of  death,  as  in  one  case  observed 
by  the  writer  in  which  the  blood-pressures  were  150  mm.  Hg  and  110  mm. 
respectively  until  the  instant  when  the  pulse  suddenly  ceased. 

PHYSICAL    EXAMINATION. 

The  appearance  of  persons  suffering  from  aortic  insufficiency  is  usually 
quite  characteristic.  The  eyes  are  bright,  with  conjunctiva  moist,  the 
pupils  often  dilated  and  palpebral  slits  wide,  giving  a  peculiar  staring  ap- 


AORTIC   INSUFFICIENCY.  367 

pearance  which  sometimes  for  an  instant  suggests  exophthalmic  goitre. 
The  sclersD  are  usually  pale  and  bluish.  The  cheeks  are  somewhat  sunken, 
the  complexion   usually  pale    and   sallow   (aortic  facias). 

One  of  the  features  which  at  once  attracts  the  attention  of  the  observer, 
as  already  the  case  with  Vieussens  in  1715,  is  the  intense  and  sudden  visi- 
ble pulsation  in  the  arteries,  especially  the  carotids,  temporals,  and 
brachials.  Often  this  pulsation  is  so  great  as  to  shake  the  entire  head, 
even  when  the  patient  is  asleep  (Frankel).  There  is  sometimes  a  visible 
pulsation  of  the  entire  uvula  (F.  Miiller)  and  of  the  arteries  in  the  retina 
(Becker) . 

Not  only  the  larger  but  also  the  smaller  arteries  pulsate  visibly,  as 
can  be  seen  in  the  so-called  capillary  pulse  (Quincke),  the  to-and- 
fro  movement  of  the  red  border  of  an  area  of  hypersemic  skin  synchronous 
with  each  pulse-wave.  This  can  be  observed  at  any  place  where  an  area 
of  erythema  borders  upon  an  area  of  pallor,  especially  along  the  margin 
of  an  area  of  skin  which  has  been  caused  to  redden  by  slight  friction,  beneath 
the  finger-nails,  or  in  the  lips  or  gums  when  gently  compressed  with  a  glass 
slide.  This  appearance  coupled  with  the  presence  of  the  bounding  and 
collapsing  pulse  is  usually  very  typical.  Indeed,  it  is  said  that  Oppolzer 
won  his  professorship  at  Vienna  by  casually  making  a  diagnosis  of  aortic 
insufficiency  while  walking  down  the  wards  of  the  hospital  and  merely 
resting  his  hand  upon  the  dorsum  of  the  patient's  foot. 

However,  Oppolzer  might  readily  have  come  to  grief  had  he  encountered  one  of  those 
not  very  rare  cases  in  which  all  these  phenomena  result  from  arteriosclerosis  alone.  Lenn- 
hoff,  V.  Weissmayer,  and  Huber  have  termed  these  cases  pseudo-aortic  insuffi- 
ciency. In  these  cases  the  arteries  are  large  and  rigid  and  there  is  a  high  pulse-pressure 
but  no  other  manifestations  of  aortic  insufficiency.  The  whole  phenomenon  is  due  to  a 
high  pulse -pressure  in  rigid  arteries  (page  261). 

The  chest  and  lungs  show  no  abnormalities  until  the  later  stages  of 
the  disease  are  reached  and  pulmonary  congestion  has  set  in  with  bronchitis, 
pulmonary  oedema,  or  hydrothorax. 

Cardiac  Impulse. — Over  the  heart  there  is  usually  some  bulging  of  the 
chest  wall,  and  usually  a  well-defined  apex  beat  in  the  fifth  or  sixth  inter- 
space to  the  left  of  the  mammillary  line.  The  impulse  is  systolic  in  time 
and  heaving  in  character  (dome-like,  "choc  en  dome"),  owing  to  the  fact 
that  the  entire  apex  is  usually  made  up  of  the  hypertrophied  left  ventricle 
(Bamberger).  In  the  second  right  interspace  there  is  often  another 
systolic  impulse,  caused  by  the  throbbing  aorta,  which  may  lead  to  the 
suspicion  of  aneurism. 

On  palpation  nothing  abnormal  is  noted  except  that  the  second  aortic 
shock  is  often  lacking.  In  about  40-50  per  cent,  of  the  cases  a  pre- 
systolic thrill  (Thayer)  and  in  15  per  cent,  a  tapping  systolic  shock 
may  be  felt  at  the  apex.  This  is  very  similar  to  that  observed  in  mitral 
stenosis  but  less  intense,  while  in  most  cases  the  impulse  is  strong  and 
heaving.  In  about  16  per  cent,  of  Thayer's  cases  an  actual  mitral  stenosis 
was  present  as  well,  and  this  association  must  always  be  borne  in  mind. 
Systolic  thrills  are  often  felt,  especially  over  the  aortic  area,  caused  by  the 
roughenings  of  the  aortic  valves,  and  also  over  the  apex  in  cases  where 
mitral  insufficiency  is  present. 


368 


DISEASES   OF  THE   HEART   AND   AORTA. 


Percussion  and  X=ray  Shadow. — As  stated  above,  the  cardiac  outline 
in  aortic  insufficiency  shows  a  marked  elongation  of  the  long  axis  (L) ,  due 
to  the  hypertrophy  and  dilatation  of  the  left  ventricle.  There  is  little 
increase  in  the  transverse  diameter  (Q),  so  that  the  area  of  cardiac  dulness 


BLOWING 

!>!  ASTOLIC  MURMUR 

BLOWING 

DIASTOLIC  MURMUR 
(AXILLARY) 
PRESYSTOLIC 
RUMBLE  (FLINT) 


Fig.  207. — Area  of  cardiac  dulness  and  distribution  of  the  cardiac  sounds  and  murmurs  in  aortic 
insufficiency.  Heavy  curved  line,  outline  of  tlie  heart;  heavy  straight  line,  longitudinal  diameter. 
Parallel  lines  indicate  the  distribution  of  the  aortic  diastolic  murmur.  Black  dot  indicates  maximum 
intensity.  Small  circle  indicates  the  distribution  of  the  presystolic  rumble  (Flint).  Small  diagram  at  the 
left  indicates  the  murmur  heard  in  each  area. 


and  the  X-ray  show  (Figs.  207,  208,  and  209)  the  form  of  a  narrow  elongated 
oval  whose  long  axis  is  inclined  more  obliquely  downward  than  is  that  of 
the  normal  heart.    In  this  way  it  presents  a  marked  antithesis  to  the  out- 


FiG.  208. — Radiograph  of  a  case  of  aortic  insuf- 
ficiency, showing  elongation  of  the  long  axis  of  the 
heart.  (Kindness  of  Prof.  C.  M.  Cooper.)  The  plate 
is  at  the  back  of  the  patient,  the  tube  in  front. 


Fig.  209.— Diagram  of  Fig.  208,  showing  the 
hypertrophy  of  the  left  ventricle.  The  broken  line 
indicates  the  normal  cardiac  outline;  the  arrow  indi- 
cates the  direction  of  enlargement;  AO  indicates 
the  shadow  of  the  dilated  aortic  arch. 


line  of  mitral  stenosis,  in  which  the  oval  is  a  broad  and  rather  short  one, 
and  to  the  broad,  elongated  oval  of  mitral  insufficiency.  The  X-ray  shadow 
often  shows  a  marked  dilatation  of  the  aortic  arch,  which  may  correspond 
to  an  area  of  dulness  in  the  second  right  interspace  and  over  the  adjacent 
portions  of  the  sternum,  but  this  can  be  differentiated  from  aneurism  bv 


AORTIC   INSUFFICIENCY.  369 

fluoroscopic  examination  with  oblique  illumination.  Indeed,  examination 
with  the  X-ray  shows  this  condition  to  be  much  more  frequent  than  had 
previously  been  suspected,  and  discloses  many  cases  of  dilated  aorta  which 
had  previously  been  regarded  as  true  aneurisms.  On  the  other  hand,  the 
tremendous  strain  upon  the  vessel  walls  in  aortic  insufficiency  tends  to 
bring  about  the  formation  of  aneurisms,  and  the  latter  is  a  relatively  fre- 
quent complication  of  aortic  insufficiency. 

The  Aortic  Diastolic  Murmur. — The  characteristic  and  almost  pathog- 
nomonic sign  of  aortic  insufficiency  is  the  blowing,  hissing,  or  occasionally 
musical  murmur  heard  over  the  heart  in  early  diastole.  This  murmur  was 
first  described  by  Hodgkin  in  1829  as  "a  constant  bruit  de  scie, 
which  presented  this  peculiarity,  that  it  was  double,  attending  the  systole 
as  well  as  the  diastole." '  However,  it  remained  for  Corrigan  (1832)  to 
recognize  its  diagnostic  significance.  The  murmur  is  caused  by  the  regurgi- 
tant stream  passing  through  the  orifice  between  the  closed  valves,  and  its 
quality,  like  the  noise  made  by  a  jet  of  steam,  depends  upon  the  size  and 
character  of  the  opening  and  the  pressure  in  the  vessel  during  diastole 
rather  than  upon  the  size  of  the  orifice.  ,  Indeed,  a  small  leak  passing 
through  a  narrow  orifice,  especially  with  irregular  and  calcified  walls,  at 
a  high  diastolic  pressure,  may  cause  a  much  more  intense  murmur  than 
a  large  leak  through  a  wide  orifice  (cf.  page  110).  Balfour  even  goes  so  far 
as  to  state  that  when  the  diastolic  murmur  is  loud  over 
the  base  but  not  over  the  carotid  artery  the  regur- 
gitation is  small,  whereas  when  it  is  loud  over  the  arteries  but  not 
heard  over  the  base  the  leak  is  a  large  one.  In  occasional  cases  of  ulcera- 
tive endocarditis  separation  of  an  entire  cusp  ma}^  occur  without  the  pres- 
ence of  the  characteristic  murmur.  Moreover,  it  is  frequently  observed 
that  the  diastolic  murmur  is  totally  absent  when  the  heart  is  rapid  and 
weak,  but  reappears  as  the  rate  falls  and  the  force  of  the  beat  increases. 
The  consistency  of  the  valves  also  plays  a  considerable  role.  A  rigid  and 
calcified  orifice  forms  a  better  sounding-board  and  gives  rise  to  a  louder 
and  more  roaring  murmur. 

As  to  the  region  in  which  it  is  best  heard,  the  statements  of  different 
authors  vary.  The  following  list  shows  the  region  of  maximum  intensity 
given  by  various  authors: 

V.  Jurgenson .Second  right  interspace  and  adjacent  portions  of 

sternum. 

Gerhardt Left  of  sternum. 

Romberg Second  and  third  left  interspaces. 

Huchard Third  right  costal  cartilage. 

Sibson Lower  part  of  left  margin  of  sternum. 

Broadbent Sternum  near  origin  of  third  left  costal  cartilage. 

Osier Midsternum,   third  costal  cartilage,   or  along  left 

border  of  sternum  as  low  as  ensiform. 

Cole  and  Cecil  have  called  attention  to  the  fact  that  in  many  cases  of 
aortic  insufficiency  the  diastolic  murmur  not  only  can  be  heard  but  under- 
goes an  accentuation  as  the  stethoscope  passes  outward  from  the  apex 
into  the  left  axilla.    The  writer  can  confirm  this  observation. 

'  Evidently  there  was  a  systolic  as  well  as  a  diastolic  murmur  present. 
24 


370 


disf:ases  of  the  heart  and  aorta. 


The  discrepancies  in  the  statements  of  the  different  observers  may  be  due  to  the 
direction  taken  by  the  regurgitant  stream.  Foster,  Balfour,  and  Grocco  suggested  that 
this  might  depend  upon  the  aortic  segment  which  happened  to  be  affected.  It  is  easy  for 
any  one  to  demonstrate  to  his  own  satisfaction  that  this  view  is  at  least  partially  correct. 
A  calf's  heart  may  be  obtained  from  a  butcher's  shop  and  a  cannula  connected  with  a  pres- 
sure bottle  inserted  into  the  aorta.  A  window  is  cut  into  the  left  ventricle,  and  a  hole  is 
then  made  in  one  of  the  aortic  leaflets.  A  regurgitant  stream  issues  froni  the  hole,  taking  a 
direction  nearly  perpendicular  to  the  plane  of  the  valve.  The  stream  emerging  from  a 
hole  in  the  left  cusp  strikes  the  septum,  that  from  the  posterior  cusp  strikes  the  left  wall 
of  the  ventricle  in  the  vicinity  of  the  apex  or  anterior  papillary  muscle,  while  that  from 
the  right  cusp  strikes  against  the  anterior  cusp  of  the  mitral  valve.  The  higher  the  pressure 
under  which  these  streams  pass  the  more  their  direction  is  deflected  toward  the  apex.  Amod- 
erate  change  in  pressure  will  make  a  great  difference  in  the  direction  taken  by  the  stream. 


Fig.  210. — Direction  of  the  primary  r^urgitant  streams  in  aortic  insuflBciency.  (Scliematic.)  I.  Re- 
gurgitant streams  passing  through  orifices  in  the  aortic  cusps.  II.  1,  Direction  taken  by  a  stream  regurgi- 
tating at  low  pressure;  2,  direction  of  stream  regurgitating  through  the  same  orifice  at  high  pressure.  III. 
A,  direction  naturally  taken  by  a  stream  regurgitating  through  an  orifice  in  the  aortic  cusp;  B,  direction 
to  which  the  stream  through  the  same  orifice  is  deflected  by  irregularities  upon  the  surface  of  the  vegetation. 


If  the  orifice  from  which  the  stream  emerges  is  an  irregular  one  like  that  at  the  margin 
of  a  vegetation,  the  direction  of  the  stream  may  be  totally  deflected  from  its  original  course 
(Fig.  210)  and  this  is  probably  the  case  in  most  clinical  conditions.  No  hard-and-fast  rules 
hold  for  all  lesions  of  any  individual  segment.  However,  the  important  fact  is  that  the 
regurgitant  stream  continues  as  a  well-defined  jet,  whose  sound  would  naturally  be  loudest 
near  the  point  where  it  strikes  and  which  would  be  transmitted  more  or  less  nearly  in  the 
direction  of  its  course.  The  walls  of  the  heart  and  the  chordae  tendineae  aid  in  transmitting 
these  murmurs  for  some  distance  beyond  their  point  of  impact. 

It  is  evident,  therefore,  that  the  mere  variations  in  the  direction  of 
the  regurgitant  streams  due  to  the  form  of  the  leak,  the  blood-pressure, 
and  the  position  of  the  heart  may  give  rise  to  the  greatest  variations  in 
the  point  at  which  the  murmur  is  maximal,  and  may  account  for  the  dis- 
crepancies in  the  clinical  findings  of  excellent  observers. 

Murmurs  over  the  Arteries. — Owing  to  the  roughening  of  the  aortic 
valves  and  sometimes  to  the  presence  of  aortic  stenosis,  a  systolic  murmur 
is  also  heard  over  the  aortic  area  and  transmitted  along  the  blood  stream 
to  the  arteries. 

In  the  carotid  and  brachial  arteries  a  diastolic  or  to-and-fro  murmur 
may  also  be  heard.  This  was  described  by  Corrigan  in  1832  and  by  Da 
Costa  Alvarenga  in  1856,  but  it  is  most  frequently  and  easily  heard  over 
the  femoral  arteries,  where  it  was  first  noticed  by  Bouillaud  and  described 
by  his  pupil,  Duroziez,  in  1861.  It  is  usually  known  as  Duroziez's 
double  murmur.  The  diastolic  portion  is  probably  due  to  a  slight 
regurgitant  stream  from  the  periphery  toward  the  larger  arteries. 


AORTIC   INSUFFICIENCY. 


371 


vol 


Flint's  Presystolic  Rumble. — Another  and  very  important  murmur  is 
the  presystolic  rumble  heard  only  at  the  apex  (Flint  murmur),  first  de- 
scribed by  Austin  Fhnt  in  1862  in  cases  of  aortic  insufficiency  without  any 
mitral    involvement.       This   rumble   is   in 
every  respect    similar  to    that    of   mitral 
stenosis,  and   it  is  extremely  difficult  to 
determine   whether   the    latter  is   absent.        pk. 

Indeed,  Flint,  in  his  original  paper,  supposed 
that  the  murmur  was  due  to  the  existence  of  a 
functional  narrowing  of  the  orifice  between  the 
mitral  cusps,  which,  as  Baumgarten  (1843)  and 
Hammernjk  had  shown,  was  closed  at  the  beginning 
of  auricular  systole.  Guiteras  and  Thayer  believe 
that  the  murmur  is  due  to  the  vibration  of  the  ante- 
rior cusp  of  the  mitral  valve  set  in  motion  by  the 
regurgitant  stream.  Thayer  and  also  Gibson  deny 
the  existence  of  such  a  functional  stenosis.  How- 
ever, the  writer  has  been  able  to  show  on  the  excised 
lieart,  by  the  method  of  Baumgarten  and  Gad,  that 
although  the  mitral  valve  usually  opens  along  its 
entire  extent,  yet  when  the  pressure  within  the  ven- 
tricle is  increased,  the  separation  of  the  cusps  occurs 
at  onlya  small  portion  of  the  lineof  closure  (Fig.212). 

An  actual  functional  stenosis  is,  there- 
fore, present  exactly  as  assumed  by  Flint. 
Snapping  First  Sound. — The  first  sound 
at  the  apex  in  30  per  cent,  of  these  cases 
has  the  snapping  character  present  in  mitral 
stenosis,  but  more  commonly  is  loud  and 

booming.     The  systolic  murmur  transmitted  to  the  left  axilla  is  present 
in  many  cases  in  which  mitral  insufficiency  is  associated. 

Aortic  Second  Sound. — When  there  is  great  destruction  or  great  retrac- 
tion of  the  aortic  cusps  and  they  do  not  ap- 
proximate, the  second  sound  may  completely 
disappear;  but  if  the  edges  are  sclerotic  or 
calcified,  or  covered  with  hard  vegetations, 
the  closure  may  even  cause  an  intensification 
of  the  second  sound,  in  spite  of  the  presence 
of  a  larger  regurgitation. 

Third  Heart  Sound. — Besides  these  sounds 
Prof.  Thayer  has  called  attention  to  the  ex- 
treme frequency  of  a  loud  third  heart  sound 
(protodiastolic  gallop  rhythm)  in  aortic  insuf- 
ficiency, associated  with  the  protodiastolic 
wave  upon  the  cardiogram.  If,  as  has  been  sug- 
gested by  Hirschfelder,  Gibson,  and  Thayer, 
this  sound  is  clue  to  the  closing  snap  in  diastole, 
it  is  quite  natural  that  it  should  be  unusually  loud  in  aortic  insufficiency 
when  the  mitral  valves  are  forcibly  clapped  together  by  the  high  diastolic 
pressure  in  the  ventricle.  It  can  be  readily  shown  on  excised  hearts  that 
the  snap  is  then  more  abrupt  than  under  normal  conditions. 


Fig.  211. — Relation  of  murmurs  in 
aortic  insufficiency  to  the  cardiac  cycle. 
PR.,  intraventricular  pressure;  VOL.,  vol- 
ume curve  of  the  ventricles.  1,  simple 
aortic  diastolic  murmur;  2,  Flint  presys- 
tolic rumble  and  aortic  diastolic  murmur; 
3,  presystolic  rumble,  diastolic  murmur, 
and  third  sound;  4,  mitral  and  aortic  in- 
sufficiency murmurs  replacing  both  sounds 
(machinery  murmur). 


mitral 


aortic 


Fig.  212. — Functional  mitral  ste 
nosis  in  aortic  insufficiency  as  demon 
strated  on  the  excised  heart  by  Baum 
garten's  method.    (Semi-schematic.) 


372  DISEASES   OF   THE   HEART   AND    AORTA. 


BLOOD-PRESSURE. 

The  blood-pressure  in  patients  with  aortic  insufficiency  presents  the 
same  characteristics  as  in  experimental  animals, — namely,  a  constantly 
high  pulse-pressure.  This  may  be  due  either  to  a  considerable 
fall  in  the  minimal  pressure  (as,  for  example,  maximal  pressure  120,  mini- 
mal 50),  as  is  most  common  in  the  endocarditic  group,  or  to  a  considerable 
rise  in  the  maximal  pressure  with  relatively  little  change  in  the  minimal 
(170  and  90  respectively),  such  as  is  usual  in  the  arteriosclerotic  form. 
Occasionally  one  encounters  cases  in  which  an  aortic  diastolic  murmur 
and  normal  pulse-rate  are  present  with  normal  maximal  and  minimal  pres- 
sures (120  and  90),  but  all  the  experimental  evidence  indicates  that  in 
these  cases  the  leak  must  be  a  small  one,  just  as  is  the  case  in  animal  experi- 
ments when  a  thrombotic  deposit  plugs  the  hole  in  a  punctured  valve 
(see  page  299).  In  such  cases,  therefore,  there  is  a  definite  lesion  of  the 
aortic  valves,  producing  but  httle  leakage  yet  a  well-marked  murmur. 
Any  disturbances  to  the  circulation  in  such  a  case  are  due  to  sclerotic  and 
myocardial  factors  rather  than  to  the  aortic  lesion.  Although  this  class 
of  cases  has  not  been  studied  extensively,  it  seems  probable  that  a  careful 
functional  diagnosis  based  upon  the  blood-pressure  findings  might  prove 
very  useful  for  prognosis. 


Fig.  213. — Variations  in  the  form  of  the  pulse-wave  encountered  clinically  in  aortic  insufficiency.     (After 
Marey.)     1,  normal  form;  2,  collapsing  (Corrigan);  3,  4,  5,  6,  anacrotic  pulse. 

PULSE. 

The  typical  pulse  of  aortic  insufficiency  is  very  characteristic,  and 
since  the  time  of  Corrigan  has  been  known  as  the  Corrigan  pulse  (water- 
hammer  pulse,  see  page  47).  The  wave  is  large,  with  a  quick  upstroke 
(pulsus    celer   et   altus)  and  sudden  fall,  leaving  the  artery  quite 


AORTIC   INSUFFICIENCY. 


373 


small  and  soft  during  diastole  (collapsing  pulse).'  In  the  typical  sphygmo- 
gram  these  characteristics  are  very  marked.  The  criterion  for  designat- 
ing a  pulse-tracing  as  collapsing  is  not  the  steepness  of  the  up-and-down 
strokes,  for  these  depend  chiefly  upon  the  speed  at  which  the  smoked  sur- 
face is  travelling,  but  lies  in  the  fact  that  the  dicrotic  notch  in  the 
collapsing  pulse  falls  below  the  middle  of  the  pulse- 
wave,  while  in  the  normal  and  anacrotic  pulse  it  lies  above  the  middle 
(Mackenzie  and  Broadbent).  Since  Marey  and  Huerthle  have  shown  that 
the  systolic  period  occupies  the  time  before  the  dicrotic  notch  and  the 


VOLUME  OF 
VENTRICLES 


VOLUME  OF 
VENTRICLES 


Fig.  214. — Tracings  from  a  dog  with  experimental  aortic  insufficiency,  showing  the  conversion  of  a 
collapsing  (A)  into  an  anacrotic  pulse  (B)  by  clamping  the  descending  aorta.  (After  Stewart.)  A,  before; 
B,  after  clamping.  The  figures  on  the  first  pulse  curves  indicate  the  time  from  the  base  to  the  summit  of 
the  pulse- wave.  The  figures  on  the  second  wave  indicate  maximal  and  minimal  pressures  in  the  carotid. 
Downstrokes  upon  the  volume  curve  represent  systole.  Clamping  the  aorta  causes  the  ventricle  to  dilate 
somewhat,  and  to  fill  more  quickly  in  diastole. 

diastolic  after  it,  it  is  but  a  paraphrase  to  state  that  in  the  collapsing  pulse 
over  half  the  fall  of  pressure  occurs  during  systole,  while 
in  the  normal  pulse  the  fall  occurs  chiefly  during  diastole.  Moreover 
the  volume  curves  by  Stewart  and  the  writer  have  shown  that  the  collapse 
occurs  while  the  blood  is  still  flowing  out  of  the  ventricle  into  the  aorta, 
and  not  at  the  time  when  the  regurgitation  is  occurring.  On  the  other 
hand,  increasing  the  peripheral  resistance,  either  by  clamping 
the  descending  aorta  or  by  the  administration  of  adrenalin,  etc.,  which 


'  Corrigan  called  attention  to  the  fact  that  elevating  the  arm  caused  the  pulse  to 
have  a  more  collapsing  quality,  but  Stewart  has  shown  that  this  is  due  to  hastening  the 
venous  return  and  not  to  increased  regurgitation.  It  can  be  prevented  by  slightly  con- 
stricting the  arm. 


374  DISEASES   OF   THE    HEART    AND    AORTA. 

caused  an  actual  increase  in  the  amount  of  blood  regur- 
gitated, caused  the  collapsing  form  of  the  pulse-wave  to 
be  replaced  by  one  of  typically  anacrotic  form  (Fig.  214). 
The  pulse-pressure,  however,  remained  high.  Moreover,  the  pulse-tracings 
of  Marey  (Fig.  213)  showed  almost  all  possible  variations  of  form  to  occur 
in  cases  of  aortic  insufficiency,  and  Stewart  found  that  the  collapsing  pulse 
was  absent  in  42  per  cent,  of  the  tracings  at  the  Johns  Hopkins  Hospital. 

There  is  also  a  certain  number  of  cases  in  which  the  clinical  note  describes 
the  pulse  as  collapsing,  while  no  such  character  appears  on  the  tracing.  In 
these  cases  there  is  usually  a  large  pulse-pressure,  and  the  discrepancy  is  due 
to  the  fact  that  the  finger  appreciates  the  amount  of  the  changes  in  pressure 
while  the  sphygmograph  records  mainly  the   suddenness   of  the  change. 

The  cause  of  the  collapsing  character  of  the  pulse  seems,  therefore,  to 
be  situated  in  the  peripheral  arteries,  though  the  relatively  small  backflow 
into  the  ventricles  and  the  high  intraventricular  pressure  during  diastole 
also  play  important  roles. 

Hasenfeld  and  Romberg  have  shown  that  these  vessels  become  greatly 
dilated  after  the  lesion  has  been  produced,  and  Stewart  has  shown  that 
this  is  due  to  a  stimulation  of  the  depressor  nerve  at  the  aortic  ring  which 
the  increase  in  intraventricular  pressure  may  render  continuous.  Eastman 
has  found  by  measurements  of  skin  temperature  that  in  typical  aortic 
insufficiency  the  peripheral  vessels  are  actually  dilated.  The  blood  there- 
fore passes  rapidly  into  the  small  arteries,  and  the  aorta  empties  itself 
rapidly,  so  that  this  factor  coupled  with  the  backflow  into  the  ventricle 
causes  the  great  fall  in  pressure  during  diastole. 

It  is  sometimes  thought  that  the  absence  of  a  collapsing 
pulse  in  a  case  of  aortic  insufficiency  indicates  the  presence  of  aortic 
stenosis.      However,   as  not  only  the  above-mentioned  experiments  but 

many  autopsy  findings 
demonstrate,  this  is  not 
the  case.  It  merely  indi- 
cates that  there  is  high 
peripheral  resistance, 
„„,.„,.,     1    .     .      ,         *•    wT>  r.\  1,    •        which  is  common  in  arte- 

FiG.  215. — Radial  pulse  tracings  from  patient  (R.  C.)  snowing         ... 

extrasystoles  [E)  which  are  probably  of  ventricular  origin.     The  riosclerosis. 

heavily  shaded  portion  represents  the  systolic  period  in  one  cardiac  Dulct^-ra^o    T'Vi 

cycle.     The  pulse  is  collapsing.  KUIJse-raie.         ine 

pulse-rate  depends  largely 
upon  the  degree  of  compensation,  being  little  faster  than  normal  in  cases 
without  symptoms,  but  usually  ranging  from  80  to  120  in  hospital  cases. 
The  pulse-rate  is  usually  regular;  but  when  the  heart's  action  is  very 
labored,  ventricular  extrasystoles  may  result  from  the  over-distention, 
and  thus  produce  an  irregular  or  a  bigeminal  pulse. 

Case  of  Aortic  Insufficiency. 

R.  M.  C,  colored  laborer,  aged  46,  entered  the  hospital  on  May  20,  1904,  complain- 
ing of  soreness  and  swelling  of  the  abdomen  and  shortness  of  breath.  He  has 
always  been  healthy  except  for  measles,  mumps,  and  whooping-cough  as  a  child,  diph- 
theria at  21,  and  chills  and  fever.  He  has  had  gonorrhoea  but  denies  syphilis. 
He  passes  water  once  a  night.  He  has  worked  hard,  exposed  to  wet  and  cold  and  doing 
heavj-  lifting.    Does  not  use  alcohol  or  tobacco. 


AORTIC   INSUFFICIENCY.  375 

About  two  years  before  admission  he  had  cough,  palpitation,  short- 
ness of  breath  on  exertion,  and  some  orthopnoea,  of  which  he  was  cured 
at  the  dispensary.  The  present  trouble  began  about  two  months  ago,  with  violent 
beating  of  the  heart  and  shortness  of  breath  which  were  worse  at  night.  These  symp- 
toms came  on  in  paroxysms,  which  may  be  produced  by  stooping  down.  He  has 
severe  paroxysmal  coughing  spells.  During  the  past  few  days  his  abdomen  has 
been   swollen,   but  his  feet  have  not  been  at  all  so. 

The  patient  is  a  poorly  nourished  man,  propped  up  in  bed  without  respiratory  dis- 
tress. There  is  marked  pulsation  visible  in  all  the  large  arteries, 
and  a  to-and-fro  murmur  can  be  elicited  over  them  by  heavy  pressure  with  the 
stethoscope.  The  lungs  are  clear  on  percussion  and  auscultation,  except  for  a  few  coarse 
mucous  rales  at  both  bases. 

Heart.  —  There  is  considerable  pulsation  over  the  precordium,  the  apex  being 
located  in  the  seventh  left  interspace  18  cm.  from  the  midline.  Dulness 
extends  upward  to  the  second  left  interspace  and  5  cm.  to  the  right  of  the  midline  in  the 
fourth  interspace.  There  is  a  well-defined  presystolic  thrill  over  the  apex. 
A  blowing  systolic  murmur  replaces  the  first  sound  and  is  heard  over  the  whole  axilla,  also 
a  short  blowing  diastolic  murmur  and  a  short  presystolic  rumble 
(Flint  murmur).  Passing  inward  and  upward  the  sounds  are  replaced  by  a  loud  to- 
and-fro  murmur,  loudest  over  the  insertion  of  the  fourth  rib  and  scarcely 
heard  to  the  right  of  the  sternum.  In  the  second  right  interspace  the  systolic  mur- 
mur is  very  harsh  and  the  first  sound  is  loud;  the  diastohc  murmur  is  well  heard. 
The  pulse  is  of  good  volume,  regular,  markedly  water-hammer  in  charac- 
ter.    Maximal   blood-pressure    170   mm.    Hg. 

Abdomen  is  full  ;  the  hepatic  dulness  extends  9  cm.  below  the  costal  margin  ; 
the  liver  is  soft  and  tender.     There  is  well-marked  oedema  of  the  legs. 

Red  blood-corpuscles  5,000,000;    hiemoglobin  75  per  cent.;    leucocytes  75  per  cent. 

He  was  put  at  rest,  soft  diet,  and  given  1  c.c.  of  tincture  of  digi- 
talis and  strychnine,  1.5  mg.  (gr.  ^5)  every  four  hours,  and  purged  freely. 
He  immediately  improved.  The  oedema  disappeared,  and  within  three  weeks  he 
was  up  and  about,  feeUng  well,  with  a  pulse-rate  of  80-90  per  minute.  He  was 
discharged  on  June  16.  His  shortness  of  breath  and  oedema  returned,  however, 
within  a  week,  and  he  re-entered  the  hospital  on  June  26  so  dyspnoeic  that 
he  was  scarcely  able  to  speak.  The  signs  were  about  as  before.  He  did  not  improve 
as  before,  however,  in  spite  of  treatment,  and  remained  dyspnoeic  throughout  the 
month,  subject  to  spells  of  intense  cardiac  asthma,  so  that  he  was  com- 
pelled to  seek  relief  by  being  propped  up  continually  in  a  wheel-chair  instead  of 
lying  in  bed.  During  this  period  his  maximal  pressure  remained  high  (150- 
17  0),  his  minimal  pressure  about  110  (Erlanger  apparatus).  During  the  after- 
noon of  August  1  the  cardiac  asthma  was  particularly  intense.  His  maximal  pressure  was 
150  mm.  Hg,  the  minimal  110.  Venesection  was  contemplated.  Before  this  could  be 
done,  however,  while  the  patient  was  being  examined  and  perfectly  conscious,  the  maximal 
blood- pressure  suddenly  fell  to  110,  the  pulse  stopped  suddenly,  and 
the  patient  dropped  back  dead. 

At  autopsy  the  aortic  segments  were  found  to  be  thickened  at 
their  edges,  and  the  valve  was  clearly  incompetent.  The  aortic  orifice  meas- 
ured 8.5  cm.  in  circumference,  the  pulmonic  8.5  cm.  The  edge  of  the  mitral  valve  was 
slightly  thickened,  the  tricuspid  also;  but  there  was  no  stenosis  of  either.  The  tricuspid 
orifice,  on  the  contrary,  measured  14  cm.  There  was  much  dilatation  and  hy- 
pertrophy of  the  left  ventricle,  the  heart  weighing  760  Gm.  The  coro- 
nary arteries  were  clear.  There  were  numerous  thrombi  along  the  walls  of 
the  right  ventricle.  Corresponding  to  this  finding  there  were  numerous  areas  of 
embolism  of  the  branches  of  the  pulmonary  arteries,  evidently  from  the  loose- 
ening  of  such  thrombi.  Along  the  pericardium  there  were  numerous  raised  irregular  pearh- 
fibrous  patches.  There  were  chronic  passive  congestion  and  oedema  of  the  lungs,  right- 
sided  hydrothorax,  chronic  passive  congestion  of  the  abdominal  viscera,  and  chronic 
gastritis. 


376  DISEASES   OF   THE   HEART   AND    AORTA. 

DIAGNOSIS. 

The  diagnosis  of  aortic  insufficiency  usually  presents  little  difficulty. 
The  following  conditions  may,  however,  give  rise  to  blowing  diastolic  mur- 
murs over  and  near  the  sternum  which  may  be  mistaken  for  aortic  insuf- 
ficiency (Cabot  and  Locke). 

1.  Dilatation  of  the  aorta. 

2.  Intense  ansDmia. 

3.  Tuberculous  mediastinitis  and  similar  conditions  (murmur  is  cardio- 

respiratory, loudest  in  inspiration). 

4.  In  association  with  mitral  disease  and  dilatation  of  the  pulmonary 

artery  (functional  pulmonic  insufficiency). 

These  conditions  are,  as  a  rule,  easily  excluded,  and  do  not  frequently 
obscure  the  diagnosis. 

On  the  other  hand,  as  has  been  seen,  it  is  often  difficult  to  exclude 
complications  such  as  mitral  stenosis  in  the  presence  of  a  well-marked 
Flint  murmur,  or  of  aortic  stenosis  when  the  pulse  is  not  collapsing. 

The  dilatation  of  the  aorta,  which  often  follows  as  a  sequela  of  aortic 
insufficiency,  is  frequently  mistaken  for  aneurism.  It  may  be  accompanied 
by  verj'  marked  pulsation  in  the  second  right  interspace  and  even  of  the  upper 
portion  of  the  sternum,  with  dulness  in  these  regions.  Even  the  X-ray  when 
taken  in  the  anteroposterior  diameter  may  be  ambiguous,  and  oblique  illumi- 
nation may  be  necessary  to  remove  the  suspicion  of  aneurism  (Holzknecht) . 

The  existence  of  a  functional  aortic  insufficiency  from  transitory 
dilatation  of  the  aortic  ring  can  only  be  definitely  diagnosed  when  an  aortic 
diastolic  murmur  and  an  abnormally  high  pulse-pressure  have  been  present 
and  have  passed  off.  This  is  indeed  a  rare  occurrence.  Other  complications 
are  few,  and  are  generally  those  of  arteriosclerosis.  Bronchial  features  may 
be  present,  as  in  any  other  form  of  cardiac  disease  when  the  pulmonary 
compensation  is  broken.  Anginal  attacks  and  coronary  sclerosis  may 
usually  be  regarded  as  a  feature  of  the  sclerotic  form  of  aortic  insufficiency 
rather  than  a  complication.  On  the  other  hand,  one  of  the  cases  under  the 
writer's  care  was  very  subject  to  severe  attacks  of  definitely  anginal  charac- 
ter, and  yet  at  autopsy  the  coronary  arteries  were  found  to  be  clear.  It  is 
possible  that  in  such  cases  the  pain  may  be  due  to  either  vasomotor  ischsemia 
or  ischsemia  due  to  the  low  mean  pressure  in  the  coronary  arteries. 

TREATMENT  AND  PROGNOSIS. 

For  purposes  of  prognosis  and  treatment  the  course  of  the  disease 
may  be  divided  into  three  stages. 

1.  Freedom  from  symptoms,  the  left  ventricle  performing 
its  work  perfectly  without  either  dilatation  or  pulmonary  stasis.  In  this 
stage  the  high  pulse-pressure,  low  diastolic  pressure,  and  collapsing  pulse 
and  throbbing  arteries  are,  nevertheless,  prominent.  The  only  indication 
is  to  aid  nature  by  avoidance  of  overstrain,  overeating,  alcohol,  coffee, 
tobacco,  unhygenic  surroundings,  and  exposure  to  infectious  diseases. 
When  hypertrophy  is  good,  the  lesion  may  persist  for  years  without  pro- 
ducing the  slightest  symptoms. 


AORTIC   INSUFFICIENCY.  377 

Three  years  ago  the  writer  examined  a  medical  student  twenty-five  years  old  who 
has  been  in  perfect  health  since  an  attack  of  rheumatic  endocarditis  at  the  age  of  ten. 
In  spite  of  his  lesion  he  has  become  an  athlete,  was  a  member  of  his  class  crew  at  Yale,  and 
excelled  in  long-distance  running;  he  smokes  and  takes  alcohol  in  moderation.  Cases 
like  this  may  persist  for  thirty-five  years  or  more  (Osier),  but  manifest  themselves  sooner 
or  later  after  infectious  diseases  or  with  the  onset  of  the  arteriosclerotic  period  of  life. 

In  cases  with  arteriosclerosis,  potassium  iodide,  0.3  Gm.  (gr.  v),  or 
sodium  nitrite,  0.2  Gm.  (gr.  iii),  three  times  a  day,  is  advisable,  to  help 
check  the  progress  of  the  arteriosclerosis  and  to  keep  down  the  blood-pres- 
sure. Occasional  Nauheim  baths,  warm  salt  baths,  or  even  ordinary  warm 
baths  are  useful  in  promoting  the  vasodilation.  Cardiac  tonicity  must  be 
maintained  at  all  costs  and  dilatation  must  be  prevented. 

2.  The  second  stage  is  that  of  dilatation  of  the  left 
ventricle.  This  is  the  stage  when  symptoms  appear,  some  arising 
in  the  sensory  nerves  of  the  ventricle  and  manifesting  themselves  in  the 
forms  described  above — palpitation,  referred  pain,  psychic  disturbances, 
anginal  attacks;  some  arising  in  the  pulmonary  circulation  as  a  result  of 
stasis,  presenting  the  various  forms  of  respiratory  disturbance.  According 
to  Head,  the  stage  of  cardiac  sensation  never  merges  into  the  stage  of  re- 
spiratory distress,  but  disappears  when  the  functional  mitral  insufficiency 
and  the  latter  symptoms  set  in.  There  is  a  "safety-valve"  action 
of  the  mitral  valve. 

As  has  been  seen,  the  important  factors  producing  distention  of  the 
ventricle  are  diminution  of  tone  and  high  peripheral  resistance.  Treatment 
should  therefore  be  directed  toward  counteracting  these  conditions.  The 
usual  cardiac  procedures,  rest,  light  diet,  free  purgation,  should  be  resorted 
to,  and,  when  improvement  warrants,  the  Nauheim  baths  and  gentle 
exercises  free  from  much  resistance. 

Digitalis  and  the  Nitrites. — The  use  of  digitahs  has  been  much  disputed. 
Corrigan  stated  that  "in  every  case  of  this  disease  in  which  digitalis  has 
been  administered  it  has  invariably  aggravated  the  patient's  sufferings." 
Broadbent  believes  that  it  should  be  used  with  caution  and  that  it  may 
even  precipitate  sudden  death,  but  that  it  is  certainly  indicated  after  mitral 
insufficiency  has  set  in.  Romberg  thinks  it  should  always  be  used  with 
caution.  It  is  probable  that  any  deleterious  property  which  the  drug  may 
possess  lies  in  its  vasoconstrictor  action,  and  hence  from  a  priori  reasons 
it  should  be  combined  with  nitroglycerin  or  other  nitrites,  or  preferably 
strophanthus  substituted.  Indeed,  strophanthus  seems  to  be  the  drug  par 
excellence  in  these  conditions,  but  with  this  drug  it  is  well  to  give  nitro- 
glycerin. The  pharmacological  researches  of  Cameron  demonstrate  that 
the  nitrites  possess  the  two  properties  most  needed  in  aortic  insufficiency, 
— that  of  increasing  tone  and  of  dilating  the  peripheral  vessels;  and  the 
writer's  clinical  experience  bears  out  the  view  that,  either  alone  or  with 
strophanthus  or  digitalis,  they  furnish  great  relief  and  are  to  be  strongly 
recommended. 

A  beautiful  series  of  animal  experiments  recently  carried  out  by 
Cloetta  merits  consideration. 

Cloetta  found  that  the  administration  of  digitalis  over  prolonged  periods  caused  no 
changes  in  size  and  strength  of  normal  rabbits'  hearts.  If  aortic  insufficiency  were  pro- 
duced and  the  animals  left  untreated  for  a  year,  their  hearts  hypertrophied  and  gained 


378  DISEASES   OF   THE   HEART    AND    AORTA. 

SO  per  cent,  of  their  original  heart  weight,  but  the  animals  lost  in  strength  and  endur- 
ance. If  they  were  treated  with  digitalis  immediately  after  producing  the  lesion,  and  the 
treatment  continued  throughout  the  year,  the  hearts  were  smaller  (hypertrophy  30  per 
cent.),  but  the  hearts  were  almost  as  strong  as  those  of  normal  rabbits.  The  aortas  of 
untreated  animals  had  widened  much  more  than  those  of  the  treated. 

Cloetta  claims  to  have  had  equally  good  results  in  patients  by  early 
and  continuous  treatment  with  digitalis,  but  the  matter  must  be  studied 
upon  a  larger  series  of  cases  before  attaining  general  acceptance.  It  is 
chiefly  applicable  to  early  rheumatic  cases,  though  it  seems  probable  that 
long-continued  administration  of  very  small  doses  of  digitalis  (0.3  c.c,  or 
5  minims,  of  the  tincture)  may  exert  this  beneficial  effect  without  pro- 
ducing the  harmful  effects  sometimes  met  with. 

For  the  extreme  palpitation  and  anginal  attacks,  little  can  be  done 
beyond  the  administration  of  amyl  nitrite  in  the  latter.  Ice-bags  to  the 
precordium  are  often  of  value,  as  is  the  Finsen  light  treatment,  galvanism 
of  the  vagus  (J.  O.  Hirschfelder) ,  etc.  Stewart  has  found  excellent  results 
after  a  lumbar  puncture,  even  when  the  cerebrospinal  pressure  was  low. 
It  is  not  unlikely  that  acupuncture  over  the  neural  segment  afflicted  might 
have  the  same  effect. 

3.  The  third  stage  is  the  stage  of  failure  of  the  right  ventricle, 
presenting  the  usual  signs  and  symptoms  except  that  anginal  attacks, 
spasms  of  cardiac  asthma,  and  Cheyne-Stokes  breathing  are  a  little  more 
common  than  in  other  diseases.  In  the  treatment  of  this  condition  the  aortic 
insufficiency  is  more  or  less  disregarded,  digitalis,  purgatives,  and  diuretics 
being  given  quite  freely.  The  administration  of  nitrites  is,  however,  still 
to  be  advised. 

What  can  be  accomplished  occasionally  in  such  cases  is  shown  by  the  case  cited  on 
page  154,  a  farmer,  aged  33  years,  who  came  under  the  writer's  care  in  November,  1903, 
entering  the  hospital  after  a  year's  suffering  with  orthopnoea  so  great  that  he  had  been 
compelled  to  sleep  in  a  chair  for  six  months,  and  oedema  and  ulceration  of  the  legs,  as 
shown  in  Fig.  123.  Under  digitalis  and  free  purgation  improvement  set  in  rapidly,  and  in 
ten  weeks  he  left  the  hospital  free  from  oedema  and  almost  free  from  dyspnoea.  He  has 
remained  quite  well,  and  has  continued  his  work  as  a  farmer  during  the  past  five  years. 

On  the  other  hand,  failure  of  compensation  is  usually  a  more  serious 
event  than  in  mitral  insufficiency,  since  the  factors  producing  weakening 
of  the  ventricles  from  over-distention  are  more  intense  and  more  persistent. 
The  writer  has  found  in  several  instances  that  broken  compensation  in 
aortic  insufficiency  is  associated  with  a  high  diastolic  pressure  which  falls 
as  the  case  improves  in  many  cases  shortly  before  death.  It  is  probable 
that  this  is  due  to  asphyxial  vasoconstriction  and  furnishes  another  example 
of  the  vicious  circle : 

(Broken  compensation  ] 
Slowed  circulation        '>       N. 
Medullary  asphyxia     ] 

{Increased  regurgitation  ]  .^  f  Vasoconstriction  ) 

Weakening  of  ventricle   j  |  Increased  peripheral  resistance  J 

Venesection  is  not  indicated  except  when  there  are  a  considerable 
grade  of  venous  stasis,  high  venous  pressure,  and  dilatation  of  the  right 
auricle;  but  in  the  writer's  experience  its  results  are  then  excellent. 


AORTIC   IXSUFFICIEXCY.  379 

In  the  anginal  attacks  and  the  spells  of  dyspnoea  or  for  insomnia, 
codein,  .03  Gm.  (gr.  h),  or  morphine,  .0075  Gm.  to  .03  Gm.  (gr.  |  to  gr.  h), 
hypodermically,  may  be  necessary,  but  should  always  be  used  as  sparingly 
as  possible,  since  the  habit  is  readily  formed  and  the  patient  injures  himself 
by  feigning  dyspnoea  in  order  to  get  the  drug. 

BIBLIOGRAPHY. 
Aortic  Insufficiency. 

Cowper:  Phil.  Trans.,  1705,  No.  299.     Quoted  from  Osier  and  Gibson,  Diseases  of  the 

Valves  of  the  Heart,  Modern  Med.,  Phila.  and  N.  Y.,  1908,  iv,  205. 
Vieiissens:  Nouvelles  decouvert«s  sur  le  coeur,  1706.    Traits  nouveau  de  la  structure  et  des 

causes  du  mouvement  natural  du  coeur,  Toulouse,  1705.    Quoted  from  Huchard,  Mai. 

du  cceur,  ;M  ed.,  Paris,  1905,  iii. 
Morgagni:  also  quoted  from  Huchard. 

Hodgkin,  T. :  On  Retroversion  of  the  Valves  of  the  Aorta.  Lond.  M.  Gaz.,  1829,  iii,  433. 
Corrigan,  D.  J.:  On  Pennanent  Patency  of  the  Mouth  of  the  Aorta  or  Inadequacy  of  the 

Aortic  Valves,  Edinb.  M.  and  S.  J.,  1832,  xxxvii,  225. 
Gillespie,  A.  L. :  An  Analysis  of  2368  Cases  admitted  with  Cardiac  Lesions  into  the  Royal 

Infirmary,  Edinburgh,  Edinb.  Hosp.  Rep.,  1898,  v,  31. 
Hasenfeld,  A.,  and  Romberg,  E.:  L^eber  die  Reservekraft  des  hypertrophischen  Herz- 

muskels,  u.s.w..  Arch.  f.  exper.  Pathol,  u.  Pharmakol.,  Leipz.,  1897,  xxxix,  333. 
Gibson,  G.  A.:  Jugular  and  Triscupid  Reflux,  Edinb.  M.  J.,  1880. 
Marey,  E.  J.:  La  circulation  du  sang  a  I'etat  physiologique  et  dans  les  maladies,  Paris, 

1881. 
Cohnheim,  J.:  Vorlesungen  ueber  allgemeine  Pathologie,  Berl.,  1882,  i. 
Jaager:  Arch.  f.  d.  ges.  Physiol.,  Bonn,  xxxi. 

Rosenbach,  O.:  Arch.  f.  exper.  Pathol,  u.  Pharmakol.,  Leipz.,  1878,  ix,  1. 
Kornfeld,  S.:  Ueber  den  Mechanismus  der  Aorten-insufficienz,  Ztschr.  f.  klin.  Med.,  Berl., 

1896,  xxix,  91,  344. 
Moritz,   F.:    Ueber  ein   Kreislaufsmodell  als    Hilfsmittel  fiir  Studium  und  Unterricht, 

Deutsch.  Arch.  f.  klin.  Med.,  Leipz.,  1899,  Ixvi,  .349. 
Stewart,  H.  A.:  Experimental  and  Clinical  Investigation  of  the  Pulse  and  Blood-j)ressure 

Changes  in  Aortic  Insufficiency,  Arch.  Int.  M.,  Chicago,  1908,  i,  102. 
Head,  H.:  On  Disturbances  of  Sensation,  with  Especial  Reference  to  the  Pain  of  Visceral 

Disease,  Brain,  Lond.,  1896,  xix,  153.    Certain  Mental  Changes  that  accompany  Vis- 
ceral Disease,  ibid,  1901,  xxiv,  345. 
Frankel:  Des  secousses  rhythmique  de  la  tete  chez  les  aortiques.  Rev.  de  Med.,  Paris, 

1902,  664. 
Miiller,  Fr.:  Pulsation  des  Gaumens  bei  Aorten-insufficienz,  Charite  Annalen,  Berl.,  1889, 

251. 
Becker:  Ueber  Retinalarterienpuls  bei   Insuffizienz   der   Aortenklappen,   Monatsschr.   f. 

Augenheilk.,  1870. 
Quincke,  H.:  Beobachtungen  ueber  Kapillar-und  Venenpuls,  Berl.  klin.  Wchnschr.,  1868. 
Lennhoff:  Ueber  P.seudoaorteninsuflfizienz,  Diss.,  Berl.,  1893. 
V.  Weissmayer,  W.:  Insuffizienz  der  Aortenklappen  ohne  Gerausch  und  Pseudoaortenin- 

suffizienz,  Ztschr.  f.  klin.  Med.,  Berl.,  1897,  xxxii,  29. 
Huber:  Ueber  Rseudoaorteninsuffizienz,  Berl.  klin.  Wchnschr.,  1898. 
Flint,  A.:  On  Cardiac  Murmurs,  Am.  J.  M.  Sc,  Phila.,  1862,  xliv,  29. 
Thayer,  W.  S.:  Observations  on  the  Frequency  and  Diagnosis  of  the  Flint  Murmur  in 

Aortic  Insufficiency,  Am.  J.  Med.  Sci.,  Phila.,  1901,  cxxii,  538. 
V.  Jurgensen,  Th.:  Valvular  Disease  of  the  Heart,  Nothnagel's  Encyclopaedia  of  Practical 

Medicine,  Amer.  edition,  trans,  by  G.  Dock,  Phila.,  1908. 
Gerhardt.     Quoted  from  v.  Jurgensen. 

Romberg,  E.:  Lehrbuch  der  Krankheiten  des  Herzens  und  der  Blutgefasse,  Stuttgart,  1906. 
Huchard,  1.  c,  Sibson,  quoted  from  Huchard. 

Broadbent,  W.  H.:  Heart  Disease  and  Aneurism  of  the  Aorta,  4th  ed.,  N.  Y.,  1906. 
Osier,  W.:  The  Principles  and  Practice  of  Medicine,  4th  ed.,  N.  Y.,  1901. 


380  DISEASES   OF   THE   HEART   AND    AORTA. 

Cole,  R.  I.,  and  Cecil,  A.:  The  Axillary  Diastolic  Murmur  in  Aortic  Insufficiency,  Johns- 
Hopkins  Hosp.  Bull.,  Baltimore,  1908,  xix,  353. 

Foster,  B.:  Essays  on  Clinical  Medicine,  Lond.,  1874. 

Balfour,  G.:  Diseases  of  the  Heart,  Lond.,  1898. 

Grocco:  Arch.  ital.  riv.  clin.,  1888.  Also  Borgherini,  A.:  Ueber  das  Verhalten  des  riick- 
laufigen  Blutstroms  bei  Insuffizienz  der  Semilunarklappen  der  Aorta,  Deutsch.  Arch. 
f.  klin.  Med.,  Leipz.,  1898,  Ix,  139. 

Eastman,  T.  J.  E.:  The  Diagnosis  of  Circulatory  Conditions  by  Temperature  Measure- 
ments, Bost.  M.  and  S.  J.,  1908,  clviii,  639. 

Holzknecht,  G.:  Die  roentgenologische  Diagnostik  der  Erkrankungen  der  Brusteinge 
weide,  Hamb.,  1901. 

Cloetta,  M.:  Ueber  den  Einfluss  der  chonischen  Digitalisbehandlung  auf  das  normale  und 
pathologische  Herz,  Arch.  f.  exper.  Path.  u.  Pharmakol.,  Leipz.,  1908,  lix,  209. 


AORTIC  STENOSIS. 


PATHOLOGICAL    ANATOMY. 

In  a  certain  percentage  of  cases  (10  per  cent.)  in  which  the  aortic  valves 
are  diseased,  the  cusps  become  fused  into  a  ring  by  which  the  orifice  into 
the  aorta  is  narrowed  (aortic  stenosis) .,  Owing  to  the  force  within  the  ven- 
tricle, this  ring  is  usually  pushed 
upward  into  the  lumen  of  the  aorta 
until  the  orifice  has  a  sort  of  dome- 
shaped  appearance  (Figs.  216  and 
217,  A). 

The  inflammatory  or  atheroma- 
tous changes  most  commonly  begin 
in  the  cusps  separately,  and  the 
process  extends  until  their  edges  be- 
come fused  with  an  organization  or 
atheroma  at  the  line  of  union.  Oc- 
casionally there  is  a  progressive 
uniform  diffuse  sclerosis  like  that 
which  often  occurs  in  mitral  lesions. 
The  condition  almost  always  arises 
from  the  same  conditions  as  aortic 
insufficiency,  but  in  rare  cases  may 
also  be  of  congenital  origin. 

Naturally  many  of  the  manifestations  depend  upon  the  degree  of 
stenosis,  which  is  sometimes  so  extreme  that  a  quill  can  barely  be  passed 


Fig.    216. 


-Specimen     showing     aortic 
\'iewed  from  above. 


Fig.  217. — Forms  of  stenotic  aortic  orificea.  A.  Lateral  view  of  the  specimen  shown  in  Fig.  210.  B, 
b.  Aortic  stenosis,  with  edges  of  cusps  flexibly  fixed  at  ring  shown  by  broken  line,  but  capable  of  move- 
ment indicated  by  arrows.     C,  c.  .Aortic  stenosis  with  rigid  cusps. 

through  the  orifice.  On  the  other  hand,  the  orifice  may  be,  relatively  speak- 
ing, wide,  and  the  valves  retain  sufficient  flexibility  to  close  it  during  dias- 
tole, so  that  a   pure    aortic   stenosis  occurs  without  any  insufficiency 

381 


382 


DISEASES    OF   THE    HEART    AXD    AORTA. 


whatever  (a  condition  present  in  about  60  per  cent,  of  the  cases).  In  the 
other  40  per  cent,  the  orifice  is  not  only  narrowed  but  the  cusps  arc  so 
fused  and  rigid  that  they  do  not  close  the  aortic  orifice  during  diastole, 
and  an  aortic  insufficiency  is  present  along  with  the  ste- 
nosis (double  aortic  lesion). 

OCCURRENCE    AND    ETIOLOGY. 

Aortic  stenosis  is  by  far  the  rarest  of  left-sided  valvular  lesions,  occur- 
ring in  only  5  per  cent,  of  the  1781  Johns  Hopkins  cases  and  in  2.73  pvv 
cent,  of  Romberg's  cases.  This  is  in  accordance  with  the  experience  of 
most  writers.  Gillespie's  statistics,  in  which  it  was  supposed  to  occur  in 
18  per  cent,  of  all  the  heart  cases  in  the  Edinburgh  Royal  Infirmary,  arc 
unique  and  arouse  the  suspicion  that  the  fault  la}'  in  the  diagnosis. 

The  etiological  factors  are  practically  the  same  as  in  aortic  insuffi- 
ciency. Syphilis  and  arteriosclerosis  play  a  relatively  important  role.  Con- 
genital stenosis  also  occurs  occasionally.  In  rare  cases  there  is  a  double 
stenosis, — one  at  the  aortic  orifice,  and  one  occurring  within  the  ventricle 
by  the  formation  of  a  fibrous  ring  from  the  septum  to  the  anterior  cusp  of 
the  mitral  valve.    The  disease  is  rare  among  women. 

PATHOLOGICAL    PHYSIOLOGY. 

The  changes  in  the  circulation  due  to  stenosis  of  the  aortic  orifice  were 
very  completely  shown  by  Liideritz  under  the  guidance  of  Prof.  Gad.  Liid- 
eritz  found  that  if  the  aortic  orifice  were  narrowed  by  the  tightening  of  a 
clamp,  the  aortic  blood-pressure  might  or  might  not  fall,  but  the  form  of  the 


Fio.  218. — Carotid  pulse  and  intraventricular  pressure  in  experimental  aortic  stenasis.  (After 
Luderitz,  Ztschr.  f.  klin.  Med.,  xx.)  |  St  marks  the  point  at  whicli  aortic  stenosis  was  produced.  The  carotid 
pulse  (CAR.)  shows  the  gradual  development  of  the  pulsus  tardus,  with  a  fall  in  blood-pressure,  while  the 
intraventricular  pressure  (INT.)  increases  tremendously. 


pulse-curve  changed.  The  upstroke  changed  from  sudden  to 
gradual  and  slanting,  ending  with  a  broad  rounded  top  whose  sum- 
mit was  reached  near  the  end  of  systole  (pulsus  tardus).  This  form  of 
pulse,  as  will  be  seen,  is  perfectly  typical  of  aortic  stenosis,  and  furnishes 
the  basis  for  the  diagnosis. 


AORTIC   STENOSIS. 


383 


Rise  of  Intraventricular  Pressure. — The  pressure  within  the  ventricle,  on  the  other 
hand,  rises  greatly,  often  as  much  at  100  per  cent.,  without  affecting  the  aortic  pres- 
sure; for  the  greater  part  of  the  contraction  is  unable  to  force  much  blood  into  the 
aorta.  The  excess  of  intraventricular  over  aortic  pressure  is  therefore  much  greater  than 
in  any  other  condition.  The  conditions  under  which  the  contraction  takes  place  conform 
more  or  less  to  those  for  the  execution  of  an  isometric  contraction,  and  the  curve  of  intra- 
ventricular pressure  comes  to  resemble  that  of  an  isometric  contraction,  the  summit 
changing  from  flat  to  the  dome-shaped,  as  is  typical  for  the  latter  (as  shown  by  Frank 
and  by  Huerthle).     That  is,  the  pres-  I 

sure  does  not  at  once  reach  its  maxi-  NORMAL  AOKTIC  STENOSIS 

mum,  but    rises  gradually,  coinciding        I        tV 

quite  well  with  the  rise  of  the  curve 
in  the  aorta.  It  is  the  direct  com- 
munication of  this  progressive  rise  of 
pressure  to  the  aorta  which  gives  rise 
to  the  pulsus  tardus,  as  well  as  the 
fact  that  the  volume  of  blood  flows 
into  the  aorta  more  slowly  than  usual. 
The  duration  of  systole  is  prolonged 
considerably,  seven  to  ten  per  cent, 
in  mild  grades  of  stenosis,  ten  to  fifty 
per  cent,  when  stenosis  is   extreme. 

When  the  ventricle  is  not 
able  to  expel  its  quota  even  by 
the  end  of  systole,  extrasystoles 
are  likely  to  occur,  and  this  fre- 
quently assumes  the  form  of 
a  continuous  bigeminal    pulse. 

Such  overfilling  of  the  left  ventricle  naturally  leads  to  stasis  in  the  auricle 
and  pulmonary  veins,  with  rise  of  pressure  in  these  parts,  pulmonary  con- 
gestion, cardiac  dyspnoea  (v.  Basch),  oedema  of  the  lungs  (Welch),  and 
secondarily  also  of  the  right  ventricle.  These  in  turn  lead  to  dilatation 
and  hypertrophy  of  the  left  ventricle  and  left  auricle  and  hypertrophy  of 
the  right  ventricle,  which  are  usually  found  to  be  present  at  autopsy. 


Fig.  219. — Diagram  of  the  circulation  showing  the 
effect  of  aortic  stenosis.  The  broken  line  indicates  the 
intraventricular  pressure.  The  vertical  black  line  indicates 
the  volume  of  the  heart,  the  shaded  portion  representing 
the  amount  of  residual  blood. 


SYMPTOMS    AND    CLINICAL    COURSE. 

Aortic  stenosis  is  probably  the  most  chronic  of  all  valvular  lesions,  and 
persists  for  years  without  affecting  the  duration  of  life.  However,  as  soon 
as  the  stenosis  becomes  marked,  so  that  the  left  ventricle  has  difficulty  in 
emptying  itself  completely,  slight  exertion,  excitement,  or  emotion  brings 
on  disagreeable  symptoms,  palpitation,  constriction,  substernal  pain  or 
anginal  attacks,  and  shortness  of  breath.  These  sensory  stimuli  probably 
arise  in  the  depressor  nerve  as  the  result  of  distention  of  the  ventricle,  for 
experiments  of  Sewall  and  Steiner  have  demonstrated  that  distention  has 
this  effect  in  animals.  The  symptoms  at  first  pass  off  when  the  patient 
rests  or  leads  a  quiet  and  hygienic  life,  but  as  the  disease  persists  they 
become  more  frequent  and  persistent.  Sudden  death  is  relatively  common, 
and  is  probably  due  to  acute  dilatation. 

Compensation. — As  in  mitral  stenosis,  compensation  is  dif- 
ficult. The  left  ventricle  may  by  increasing  its  power  continue  to  drive 
enough  blood  into  the  aorta  to  maintain  the  blood-pressure,  and  even  to 
cause  the  pulse  to  resume  the  normal  form  (Fig.  223),  but  this  is  done  at 


384 


DISEASES   OF   THE    HEART   AND    AORTA. 


an  enormous  waste  of  energy,  which  sooner  or  later  brings  on  heart  failure. 
Moreover,  the  lesion  itself  is  slowly  progressive,  and  this  constantly  increases 
the  difficulty  of  maintaining  the  circulation.  In  the  final  stage  broken 
compensation  sets  in  exactly  as  in  other  advanced  valvular  lesions. 

When  aortic  insufficiency  coexists  the  circulatory  difficulty  is  naturally 
increased,  since  the  ventricle  must  drive  an  even  excessive  amount  of  blood 
into  the  aorta  in  order  to  maintain  the  circulation,  in  spite  of  the  difficulty 
under  which  it  already  labors.  Moreover,  these  are  often  the  cases  with  the 
most  advanced  pathological  lesions,  so  that  the  coexistence  of  aortic  insuffi- 
ciency renders  the  prognosis  less  favorable  than  that  of  pure  aortic  stenosis. 


;  PHYSICAL    EXAMINATION. 

The  most  striking  feature  upon  general  physical  examination  in  aortic 
stenosis  is  the  presence  of  a  well-marked  systolic  thrill  and  bruit  over  the 
larger  arteries.  Over  the  chest  there  is  usually  a  certain  amount  of  pre- 
cordial bulging.  The  apex  impulse  is  sometimes  well  marked  and  heaving, 
situated  quite  outside  the  mammillary  line  in  the  fifth  or  sixth  interspace; 
frequently,  however,  it  is  not  visible  nor  palpable.    Between  the  apex  and 

the  sternum  there  is  often  some 
systolic  retraction  of  the  inter- 
spaces from  the  contraction  of 
the  hypertrophied  right  ventri- 
cle. The  left  ventricle  hypertro- 
phies, increasing  in  size  along  its 
long  axis  (obliquely  downward) . 
Palpation.  —  Palpation  re- 
veals a  systolic  thrill  which  is 
usually  very  marked  and  felt 
over  the  whole  heart,  especially 
over  the  aortic  area.  It  is  pres- 
ent in  the  carotid  and  brachial 
arteries,  and  is  transmitted  in 
the  direction  of  the  blood  stream 
(see  page  92).  The  intensity 
of  this  thrill  is  often  the  most 
striking  feature  of  all  the  phys- 
ical signs,  and  may  far  exceed 
that  which  is  found  in  any  other 
condition.  The  shock  of  the  first  sound  is  usually  felt,  while  that  of  the 
second  is  often,  though  not  always,  absent. 

Percussion  and  X=ray  examination  reveal  no  peculiarities  other  than 
an  area  of  cardiac  dulness  enlarged  along  its  longitudinal  axis,  as  in  aortic 
insufficiency;  but,  owing  to  the  presence  of  functional  mitral  insufficiency 
and  dilatation  of  the  conus  arteriosus,  the  area  of  dulness  may  be  higher 
and  broader  than  in  aortic  insufficiency  and  resemble  that  found  in  organic 
mitral  insufficiency. 

Auscultation. — On  auscultation  one  is  immediately  struck  by  the  pres- 
ence of  a  loud  systolic  murmur  most  intense  over  the  aortic 
area,  and    transmitted   thence   to   the   first    right   inter- 


FiG.  220. — Diagram  showing  the  cardiac  outline  and 
distribution  of  the  murmur  in  aortic  steno^iis.  The  par- 
allel shading  indicates  the  distribution  of  the  systolic 
murmur  and  thrill;  the  dot  indicates  the  point  at  which 
they  are  most  intense. 


AORTIC   STENOSIS. 


385 


space  and  along  the  course  of  the  arteries,  where  it  is, 
as  a  rule,  still  loud  and  distinct.  It  is  also  heard  over  the  pulmonic  area, 
body  of  the  heart,  and  over  the  apex,  but  far  less  loudly  than  in  the  aortic 
area  and  the  arteries. 

This  murmur  is  usually  the  loudest  that  is  heard  in  any  form  of  valvular 
disease,  and  is  often  heard  several  feet  away  from  the  patient.  The  mechan- 
ism of  its  production  exemplifies  perfectly  the  simple  experiment  for  the 
production  of  thrills  and  murmurs  described  on  page  92.  Since  it  cannot 
be  produced  until  the  blood 
begins  to  flow  into  the  aorta, 
this  murmur  does  not  begin 
until  an  appreciable  in- 
terval after  the  begin- 
ning of  systole  (Boy- 
Teissier,.  Romberg,  Weiss  and 
Joachim)  and  follows  the 
first  sound  in  that  region 
as  well  as  at  the  apex  (Fig. 
221).  Weiss  and  Joachim  have 
recorded  this  murmur  with  their 
phonoscope,  and  find  that  it 
sets  in  with  a  crescendo  char- 
acter at  the  very  end  of  the  first 
sound.  The  crescendo  continues 

until  the  crest  of  the  carotid  pulse,  after  which  it  changes  to  decrescendo 
throughout  the  rest  of  systole.  The  form  of  the  carotid  wave  portrays  the 
amplitude  of  the  vibrations  and  the  variations  in  loudness  of  the  murmur. 
When  mitral  insufficiency  (organic  or  functional)  is  present,  the  mitral 
murmur  may  enter  into  or  replace  the  first  sound. 

The  second  sound  may  vary  considerably  in  aortic  insufficiency. 
If  the  valves  are  fused  throughout  their  whole  extent,  it  will  be  entirely 
absent;  but  if  portions  of  the  cusps  remain  freely  movable  their  closure 
may  give  rise  to  a  sound.  Owing  to  the  small  excursion,  this  sound  may 
not  be  as  loud  as  it  would  be  if  no  stenosis  were  present,  but  this  factor 
may  be  more  than  balanced  by  the  presence  of  sclerotic  plaques  and  calcifi- 
cations whose  concussions  may  actually  render  the  second  sound  louder 
than  normal. 


CAROTID 


SOUNDS 


rio  SEC. 


1  MUR  2         1 

Fig.  221. — Murmur  of  aortic  stenosis.  (After  Weiss 
and  Joachim.)  Upper  curve,  carotid  pulse;  middle  curve, 
heart  sounds;  lower  curve,  time;  one  vibration  equal 
to  iJn  second.  The  second  sound  is  practically  absent. 
The  murmur  is  composed  of  a  crescendo  followed  bj-  a 
decrescendo  character  loudest  with  the  upstroke  on 
the  pulse-wave. 


PULSE. 

Aortic  stenosis  may  be  said  to  be  the  only  disease  in  which  the  absolute 
diagnosis  is  determined  by  the  pulse-tracing.  The  pulse  is  small,  hard 
(high  diastolic  pressure),  and  in  typical  cases  rises  and  falls  very  slowly 
(pulsus  tardus).  Like  the  curves  in  experimental  aortic  stenosis  (Fig.  219), 
the  typical  radial  pulse-curve  (Fig.  222)  shows  a  very  oblique  ascent 
which  lasts  throughout  systole,  the  summit  of  the  curve  appearing  just  be- 
fore the  dicrotic  notch.  This  is  produced  by  the  slow,  gradual,  and  progres- 
sive filling  of  the  arteries  from  the  gradually  increasing  intraventricular 
pressure.  It  may  be  recalled  that  during  the  period  of  tlie  up-stroke  upon 
the  pulse-wave  blood  is  flowing  into  the  aorta  more  rapidly  than  onward 

.  25 


386 


DISEASES   OF   THE    HEART    AND    AORTA. 


to  the  periphery;  that  during  the  period  of  the  plateau  the  inflow  and  out- 
flow are  equal;  and  during  the  period  of  fall  blood  is  flowing  onward  to  the 
periphery  more  rapidly  than  it  flows  into  the  aorta. 

The  pulse  of  aortic  stenosis,  there- 
fore, reflects  the  true  condition,  that 
blood  is  flowing  into  the  aorta  less 
rapidly  than  usual  and  out  of  it  also 
less  rapidly.  However,  it  must  be 
admitted  that  this  typical  form  of 
pulse  is  rather  rare.  Most  commonly, 
either  the  aortic  stenosis  does  not  reach 
this  stage  without  being  complicated 
by  an  insufficiency  which  changes  the 
pulse  form  or  death  intervenes  before 
these  signs  of  inability  of  the  heart 
to  empty  itself  have  set  in.  Indeed,  many  practitioners  may  pass  through 
long  lives  of  busy  practice  without  encountering  a  single  example  of  aortic 
insufficiency  with  pulsus  tardus.     The  anacrotic  pulse  is  so  much  more 


Fig.  222. — Diagram  showing  the  pulsus  tar- 
dus and  the  anacrotic  type.  Solid  line,  pulsus 
tardus,  showing  the  slow  gradual  rise;  broken 
line  showing  the  anacrotic  form  with  sudden 
almost  vertical  rise  surmounted  by  a  plateau 
which  takes  up  the  greater  part  of  systole. 


VII 


Fig.  223. — Pulse  tracings  from  cases  of  aortic  stenosis.  The  heavily  shaded  curve  represents  the  sys- 
tolic portion  of  the  tracing.  I.  Anacrotic  pulse  from  a  case  of  tricuspid  insufficiency  but  no  aortic  stenosis, 
showing  quick  upstroke  with  only  the  summit  sloping.  II,  III.  Pulsus  tardus  from  a  case  of  aortic  ste- 
nosis (L.  S.),  IV.  Tracing  from  a  case  of  aortic  stenosis  and  insufficiency.  V,  VI,  VII.  Tracings  from 
another  case  of  aortic  stenosis  and  insufficiency.  V.  Taken  on  February  28  soon  after  admission ;  symptoms 
of  cardiac  weakness  well  marked;  maximal  blood-pressure  130  mm.  Hg.  The  upstroke  is  gradual  and  slop- 
ing. VI.  From  same  patient  on  March  24  after  recovery  from  cardiac  symptoms.  Maximal  pressure  160. 
The  strong  heart  forces  blood  rapidly  through  the  stenosed  orifice  and  causes  a  sudden  upstroke.  VII. 
Pulse  tracing  taken  immediately  after  VI,  with  other  arm  raised.  The  increased  resistance  changes  the 
tracing  to  a  pulsus  bisferiens. 

common  in  aortic  stenosis  that  examples  of  it  are  given  in  many  text-books 
erroneously  labelled  pulsus  tardus.  A  pulse-curve  with  a  sud- 
den perpendicular  up-stroke,  however,  is  not  a  pulsus 
tardus ,  but  an  anacrotic  pulse,  whatever  may  be  the  form  of  its  summit. 


AORTIC   STENOSIS.  387 

It  indicates  that  blood  is  flowing  into  the  aorta  from  the  heart  more  rapidly 
than  it  is  flowing  out  of  the  aorta  toward  the  periphery,  a  condition  which 
occurs  in  aortic  stenosis  only  (1)  when  the  orifice  is  so  slightly  narrowed 
that  the  hypertrophied  left  ventricle  is  able  to  drive  blood  through  it  with 
great  rapidity,  and  (2)  when  the  peripheral  vasoconstriction  is  so  great  that, 
in  spite  of  a  slow  inflow  into  the  aorta,  the  blood  still  enters  the  latter  much 
more  rapidly  than  it  can  leave  it.  The  former  is  the  more  common  condi- 
tion; and  it  would  appear  that  the  hypertrophy  of  the  ventricle  can  usually 
keep  pace  with  the  advancing  stenosis  until  a  very  late  stage  is  reached. 
The  pressure  within  the  ventricle  produced  under  these  conditions  is  prob- 
ably tremendous. 

These  facts  are  well  illustrated  in  Curves  V,  VI,  VII  (Fig.  223).  The  first  (V)  was 
taken  when  the  patient's  heart  was  weak,  and  the  blood-pressure  shows  a  gradual  up-stroke 
and  is  fairly  typical  of  aortic  stenosis.  The  other  curves  (VI  and  VII),  taken  after  his 
heart  had  improved,  have  taken  on  the  characters  of  aortic  insufficiency  and  have  lost  those 
of  aortic  stenosis. 

Arrhythmia. — The  rhythm  of  the  heart  in  man,  as  in  animal  experi- 
ments, is  frequently  irregular;  small  beats  and  dropped  beats  being 
frequent,  due  to  the  occurrence  of  a  pulsus  alternans  or  to  extrasys- 
toles  arising  in  the  left  ventricle  when  that  chamber  is  unable  to  empty 
itself  sufficiently.  Exercise,  emotion,  or  any  other  form  of  cardiac  over- 
strain, on  the  one  hand,  or  of  cardiac  weakening,  on  the  other,  precipitates 
this  irregularity. 

BIood=pressure.  —  The  blood-pressure  in  aortic  stenosis  is  usually 
slightly  elevated  (maximal  pressure  130  to  160  mm.),  due  in  part  to  the 
accompanying  arteriosclerosis,  in  part  to  the  increase  in  the  intraventricular 
pressure,  especially  when  the  heart  hypertrophies. 

DIAGNOSIS. 

In  typical  cases  the  diagnosis  of  aortic  stenosis  is  extremely  simple. 
The  presence  of  slow,  gradual  pulse,  the  pulse-tracings,  the  enlarged  heart, 
the  very  intense  systolic  thrill,  the  thrill  and  murmur  over  the  aortic  area 
and  arteries,  and  the  absence  or  marked  diminution  of  the  aortic  second 
sound,  present  a  perfectly  characteristic  picture.  In  certain  cases,  however, 
and  especially  when  there  is  arteriosclerosis  or  aortic  insufficiency,  it  may 
become  extremely  difficult  to  decide  whether  a  mild  grade  of  stenosis  is 
present. 

Case  op  Aonxic  Stenosis. 

Mrs.  L.  S.,  housewife,  aged  58,  entered  the  Johns  Hopkins  Hospital,  April  29,  1904, 
complaining  of  heart  trouble.  She  has  always  been  healthy;  has  had  no  infectious  diseases 
and  never  had  rheumatism,  but  occasionally  has  had  sore  throat.  She  has  occasionally 
had  fainting  spells  and  palpitation  after  mental  excitement,  and  during 
the  past  year  has  had  to  void  three  or  four  times  a  night.  Except  for  these  symptoms  she 
was  quite  well  until  a  year  before  admission,  when  one  night  after  a  heavy  meal  she  awoke 
with  extreme  dyspnoea,  palpitation,  and  a  feeling  of  extreme  weakness.  She  had  no  pain, 
but  felt  considerably  alarmed.  Immediately  after  this  her  feet  became  swollen 
and  in  spite  of  a  sojourn  in  bed  she  became  subject  to  attacks  of  extreme  dyspnoea.  The 
oedema  of  the  feet  subsided,  however,  but  reappeared  after  exertion. 

At  the  time  of  examination  the  patient  was  propped  up  in  bed,  with  slight 
dyspnoea.      She  was  fairly  nourished,  pale,  sallow,  lips    very   cyanotic.      Lungs 


388  DISEASES   OF   THE    HEART    AND    AORTA. 

clear  on  percussion  and  auscultation,  except  at  both  bases,  where  the  note  is  impaired  and 
the  breath  sounds  are  accompanied  by  crackHng  rales. 

Heart.  —  The  apex  impulse  is  barely  visible  in  the  sixth  left  interspace 
13  cm.  from  the  midhne,  from  which  point  dulness  extends  upward  to  the  third  rib, 
as  well  as  3  cm.  to  the  right  of  the  midline.  There  is  slight  impairment  of  the  percussion 
note  over  the  sternum.  A  soft  systolic  murmur  is  heard  at  the  apex  and  in  the 
axiUa,  becoming  louder,  however,  as  the  sternum  is  approached,  and  maximal  over 
the  second  right  interspace,  where  it  becomes  rough  in  character.  It  is 
transmitted  to  the  carotids  but  not  to  the  subclavians.  The  second  pul- 
monic sound  is  louder  than  the  second  aortic.  There  is  a  well-marked  thrill 
over  the  base  and  manubrium,  most  marked  in  the  second  right  interspace. 
Slight  pulsation  over  the  manubrium.  No  tracheal  tug.  The  pulse  is  small, 
regular,  100  per  minute.  The  left  radial  pulse  is  a  trifle  larger  than  the  right.  Tracing 
shows  a  well-marked  pulsus  tardus  (Fig.  I  and  II).  Blood-pressure  150 
m  m .   Hg. 

The  abdomen  is  distended  but  does  not  contain  fluid.    The  legs  are  very  cedematous. 

Urine  is  reddish;  specific  gravity  1030;  acid,  and  contains  a  large  number  of 
hyaline   casts. 

Red  blood-corpuscles  5,300,000;   haemoglobin  85  per  cent.;  leucocytes  10,000. 

During  the  first  week  she  improved  under  rest,  purgation,  and  digi- 
talis; but  on  May  8  had  a  severe  spell  of  dyspnoea  not  controlled  by  morphine 
or  nitroglycerin,  but  somewhat  relieved  by  strychnine,  3  mg.  {4(j  gr.  hypo.).  During  the 
attack  the  aortic  murmur  was  much  less  marked  than  it  had  been  before. 
The  cardiac  outlines  were  unchanged.  There  was  very  slight  development  of  fresh 
rales,  indicative  of  pulmonary  oedema.  After  the  attack  and  the  nitroglyc- 
erin there  was  unequal  dilatation  of  the  peripheral  venules.  Cheyne-Stokes  respiration 
developed  during  the  night.  A  few  purpuric  areas  were  seen  over  the  extremi- 
ties and  the  sacrum. 

On  the  next  day  she  had  another  attack  of  dyspnoea,  aft-er  which  cyanosis  deepened, 
respiration  became  labored,  the  pulse  weakened,  and  the  blood-pressure  fell  gradually 
until  the  patient  died  in  the  early  evening. 

At  autopsy  the  three  aortic  cusps  were  found  to  be  fused  together 
by  a  calcareous  cement,  leaving  an  orifice  notmore  than  3  mm.  in 
diameter.  The  left  ventricle  was  markedly  hypertrophic,  the  right 
less  so.  Both  were  dilated.  The  heart  weighed  600  Gm.  There  were  slight  atheroma  of 
the  aorta  below  the  transverse  arch,  infarction  and  oedema  of  the  lungs,  left  hydrothorax, 
left  pleural  adhesions,  chronic  passive  congestion  of  the  liver  (nutmeg),  spleen,  and  kid- 
neys; general  anasarca. 

TREATMENT. 

As  regards  treatment  there  is  little  to  be  said.  Fortunately,  the  disease 
is  very  chronic  in  its  course,  especially  when  it  begins  after  the  period  of 
adolescence  has  passed.  A  quiet  life  under  the  best  possible  hygienic  con- 
ditions, with  avoidance  of  infections,  excitement,  and  all  forms  of  stimulants 
and  overstrain,  usually  serves  to  stave  off  the  onset  of  symptoms  for  many 
years.  When  these  once  appear  in  spite  of  quiet,  the  case  is  practically 
hopeless.  Absolute  rest,  light  diet,  moderate  purgation,  and  lessening  of 
the  peripheral  resistance  by  means  of  the  nitrites  and  the  Nauheim  baths 
constitute  the  most  important  means  of  treatment.  Digitalis  is  of 
value  until  the  heart  reaches  its  limit  of  hyjDertrophy,  after  which  it  merely 
precipitates  overwork  and  irregularity  of  the  heart. 

In  the  acute  attacks  of  acute  heart  failure,  venesection  should  be 
resorted  to  promptly,  in  order  to  lessen  the  residual  blood  in  the  left  ven- 
tricle by  diminishing  the  inflow  into  it. 


AORTIC   STENOSIS.  389 

BIBLIOGRAPHY. 

Aortic  Stenosis. 

Romberg,  E.:  Lehrbuch  der  Krankheiten  des  Herzens  imd  der  Blutgefasse,  Stuttgart, 

1906. 
Gillespie,  A.  L. :    An  Analysis  of  2368  Cases  Admitted  with  Cardiac  Lesions  into  the  Royal 

Infirmary,  Edinburgh,  during  the  Five  Years  1891-1896,  Edinb.  Hosp.  Rep.,  1898, 

V,  31. 
Ltideritz,  C:  Versuche  ueber  den  Ablauf  des  Blutdrucks  bei  Aortenstenose,  Ztschr.  f. 

klin.  Med.,  Berl.,  1892,  xx,  373. 
Welch,  W.  H.:  Zur  Pathologie  des  Lungenoedems,  Arch.  f.  path.  Anat.,  etc.,  Berl.,  1878, 

Ixxii,  375. 
Sewall,  H.,  and  Steiner,  D.  W.:  A  Study  of  the  Action  of  the  Depressor  Nerve,  etc.,  J. 

Physiol.,  Camb.,  1885,  vi,  162. 
Boy-Teissier:  L'auscultation  retrosternale,  Rev.  de  M^d.,  Par.,  1892,  xii,  169. 


VI. 
PULMONARY  INSUFFICIENCY. 

Insufficiency  of  the  pulmonary  orifice  usually  occurs  either  as  a  con- 
genital lesion  or  as  a  result  of  a  severe  endocarditis  in  which  other  valves 
are  involved.  Even  as  such  it  is  a  very  rare  disease,  only  3  cases  having 
been  seen  among  24,000  admitted  to  the  medical  service  of  the  Johns  Hop- 
kins Hospital. 

Lesions  of  the  pulmonary  valves  had  been  described  by  Morgagni,  but 
the  first  clinical  cases  of  pulmonary  insufficiency  were  described  by  Norman 
Chevers  in  1846,  and  after  him  by  Frerichs,  Benedikt,  Walshe,  and  Stokes. 
Barie  in  1891  was  able  to  collect  detailed  records  of  58  cases  with  24 
autopsies. 

PATHOLOGICAL    ANATOMY. 

The  conditions  leading  to  regurgitation  at  the  pulmonary  orifice  may 
be  divided  into  six  groups: 

I.  Congenital  malformations  of  the  valve  resulting  in 
atrophy  and  deformity.  The  presence  of  only  two,  or,  on  the  other  hand, 
of  four  cusps  does  not  usually  bring  about  any  leakage.  In  this  category 
may  also  be  mentioned  stenosis  of  the  orifice. 

II.  Endocarditic  vegetations  upon  the  valves,  especiallj' 
arising  in  very  acute  attacks  of  endocarditis  with  lesions  of  other  valves. 

III.  Arteriosclerotic  changes  in  the  cusps,  often  associated 
with  dilatation  and  arteriosclerosis  of  the  pulmonary  artery. 

IV.  Aneurisms   of    the    cusps. 

V.  Ruptures  of  the  cusps  during  coughing  or  strain,  especially  of 
cusps  already  diseased. 

VI.  Dilatation  of  the  pulmonary  artery  and  conus  arteriosus  lead- 
ing to  a  functional    insufficiency  of  the  valves. 

According  to  many  writers,  especially  Gibson,  a  functional  insuffi- 
ciency of  the  pulmonary  valve  of  more  or  less  transitory  duration  takes 
place  as  a  result  of  dilatation  of  the  artery  and  of  the  right  ventricle. 
This  would  naturally  occur  most  frequently  in  cases  of  mitral  stenosis 
with  broken  pulmonary  compensation,  and  would  account  for  the  blow- 
ing diastolic  murmur  which  is  sometimes  heard  to  the  left  of  the  sternum 
in  these  cases. 

The  experimental  data  upon  this  subject  are  more  or  less  uncertain.  G.  A.  Gibson  has 
shown  upon  the  dead  heart  that  the  pulmonary  valves  become  insufficient  under  much  lower 
pressures  than  are  necessaay  to  cause  leaks  at  the  aortic.  He  has  also  shown  that  these 
leaks  can  be  prevented  from  occurring  in  the  dead  heart  if  the  pulmonary  orifice  be  pre- 
vented from  dilating  (as  by  surrounding  it  with  a  string).  His  studies  would  therefore 
lead  one  to  believe  that  such  regurgitations  would  occur  readily  in  hearts  whose  tonicity 
was  diminished  and  in  which  the  fibres  about  the  pulmonary  orifice  stretched  accordingly. 
390 


PULMONARY   INSUFFICIENCY. 


391 


On  the  other  hand  Sollman  has  shown  in  the  hving  excised  cat's  heart  perfused  with  Ringer's 
solution  and  other  salt  mixtures  that  the  pulmonary  orifice  can  withstand  tremendous 
pressure  without  leaking. 

However,  Stokes,  Kolisko,  Bristowe,  Coupland,  Litten,  Chauffard, 
Gouget  and  Preble,  have  reported  cases  of  relative  pulmonary  insufficiency, 
supported  by  autopsy.  In  all  these  cases  there  was  dilatation  of  the  right 
ventricle,  and  in  three  of  them  a  mitral  lesion  with  pulmonary  stasis.  It 
seems  quite  likely,  moreover,  that  such  a  pulmonary  insufficiency  was 
present  in  cases  W.  H.  (page  402)  and  B.  I.  (page  417),  though  the  water 
test  was  not  applied  to  the  valves  at  autopsy. 


ETIOLOGICAL    FACTORS. 

Barie's  statistics  collected  from  50  cases  of  organic  pulmonary  insuf- 
ficiency show  that  the  two  sexes  are  affected  with  equal  frequency.  It  was 
found  in  patients  of  all  ages  from  birth  to  75  years,  but  37  out  of  46  cases 
(80  per  cent.)  occurred  between  the  ages  of  18  and  34  years.  In  40  per  cent, 
the  disease  was  congenital,  but  in  these  it  never  occurred  as  the  sole  lesion, 
being  usually  associated  with  stenosis.  Rheumatism  was  the  etiological 
factor  in  16  per  cent,  of  the  cases.  Puerperal  infection,  gonorrhoea,  and 
the  other  infectious  diseases  rank  next  in  frequency.  There  is  also  an 
arteriosclerotic   group    due    to 

syphilis,     alcohol,    and     other  normal  m<j^^^r,lV^v 

affections  especially  associated 
with  mitral  stenosis  and  scle- 
rosis of  the  pulmonary  artery. 

pathological  physiology. 

Pulmonary  insufficiency 
bears  the  same  relation  to  the 
lesser  circulation  that  aortic 
insufficiency  bears  to  the  sys- 
temic circulation.  The  effect 
of  the  leak  is  to  bring  about  a 
lowered  diastolic  pressure  and 
an  increased  pulse-pres- 
sure in  the  pulmonary 
artery,  accompanied  by  a 
somewhat  greater  systolic  out- 
put from  the  right  ventricle  to  compensate  for  the  leak.  The  increased 
intraventricular  pressure  in  the  right  ventricle  during  diastole  gives  rise  to 
hypertrophy  when  the  strain  is  compensated,  and  dilatation  when  the 
strain  becomes  too  great.  As  a  result  of  this  dilatation,  functional 
insufficiency    of    the    tricuspid    valve  very  readily  sets  in. 

The  results  of  these  secondary  changes  are,  therefore: 

1.  To  slow  the  circulation  through  the  lungs. 

2.  To  cause  a  marked  rise  of  pressure  and  stasis  in  the  systemic  veins. 

3.  When  this  occurs  less  blood  enters  the  left  ventricle  than  before.  This  would 
naturally  lead  to  a  fall  in  blood-pressure;  but,  just  as  in  mitral  stenosis,  it  is  compensated 


Fig.  224. — Diagram  of  the  circulation  in  pulmonary- 
insufficiency.  I.  Normal.  II.  Moderate  grade  of  pul- 
monic  insufficiency. 


392 


DISEASES   OF   THE   HEART    AND    AORTA. 


by  constriction  of  the  peripheral  vessels  and  the  blood-pressure  maintained.  The  vaso- 
constriction, however,  manifests  itself  in  the  smallness  of  the  arteries  and  of  the  pulse,  which 
thus  presents  a  striking  contrast  to  the  pulse  of  aortic  insufficiency.  The  pulse-pressure 
also  is  never  increased,  as  is  the  rule  in  the  latter  condition. 


SYMPTOMS. 

The  symptoms  and  complications  are  chiefly  respiratory  in  origin: 
dyspnoea,  especially  in  intense  paroxysms  which  are  brought 
about  by  slight  exertion;  cough  and  bronchitis,  resulting  from  the  poor 
circulation  through  the  lungs.  The  intense  pulsation  of  the  pulmonary 
vessels  weakens  their  walls  and  predisposes  to  haemoptysis  and  the 
expectoration  of  blood-tinged  sputum.    Phthisis  is  a  common  complication. 

Palpitation  is  sometimes  noted. 
Anginoid  attacks  and  pressure 
at  the  base  of  the  sternum  are 
frequently  met  with;  also  pain, 
which,  in  contrast  to  that  aris- 
ing in  aortic  insufficiency,  is 
more  commonly  referred  to  the 
right  shoulder  and  down  the 
right    arm. 

Sudden  death  is  rela- 
tively common,  sometimes  re- 
sulting from  over-distention  of 
the  right  ventricle,  sometimes 
from  embolism  in  the  pulmo- 
nary artery. 


Fig.  225. — Distribution  of  the  murmur  in  pulmo- 
nary insuflficiency.  The  parallel  shading  indicates  the 
area  over  which  the  murmur  is  heard.  The  dot  indicates 
the  point  at  which  it  is  loudest;  the  diagram  at  the  right 
indicates  its  position  in  the  cardiac  cycle.  The  diagrams 
over  the  shaded  area  represent  the  pulsations,  i.  e.  the 
systolic  impulse  over  the  pulmonary  area  and  the  systolic 
retraction  over  the  right  ventricle. 


PHYSICAL    SIGNS. 


Cyanosis,   as  a  result  of 

the    slowed    circulation    in    the 

lungs,  is  one  of  the  earliest  signs. 

It  is  usually  very  marked  and 

is    liable    to    occur    in    paroxysms.      Signs    of    bronchitis    or    often    of 

bronchopneumonia    are   found    in    the    chest. 

Examination  of  the  heart  shows,  as  a  rule,  some  precordial  bulging, 
with  well-marked  pulsation  of  the  conus  arteriosus  in  the  second 
left  interspace,  and  a  systolic  retraction  in  the  third,  fourth,  and  fifth  left 
interspaces  and  epigastrium,  due  to  the  vigorous  beating  of  the  right  ven- 
tricle. The  area  of  cardiac  dulness  is  increased  to  the  right  in  the  trans- 
verse diameter,  owing  to  dilatation  of  the  right  auricle.  Very  often  it 
extends  upwards  in  the  second  left  interspace  as  well  (dilated  conus  arterio- 
sus), where  it  extends  5-6  cm.  to  the  left  of  the  midline.  The  area  of 
cardiac  flatness  is  increased  to  both  left  and  right,  and  forms  a  scalene 
triangle  extending  to  the  right  border  of  the  sternum.  On  palpation  the 
vigorous  beating  of  the  conus  arteriosus  may  be  felt  in  the  second  left 
interspace,  also  a  diastolic  or  systolic  and  diastolic  thrill  in  this  region  and 
over  the  right  ventricle.  On  auscultation  the  sounds  at  the  apex  may  be 
clear.    The  characteristic  feature  is  the  presence  of  a  very  superficial  dias- 


PULMONARY   INSUFFICIENCY.  393 

tolic  murmur  maximal  over  the  pulmonary  area,  varying  from  short  and 
soft  to  loud,  rough  and  hissing  in  character  and  not  infrequently  musical. 
It  is  also  heard  along  the  left  sternal  margin,  but  less  distinctly  over  the 
aorta.  The  difference  is  accentuated  on  coughing.  Owing  to  the  presence 
of  other  lesions  in  the  pulmonary  artery,  there  may  also  be  a  loud  systolic 
murmur  at  the  base,  while  over  the  base  of  the  sternum  a  systolic  mur- 
mur, due  to  the  secondary  tricuspid  insufficiency,  may  also  be  present. 

The  pulse,  in  contrast  to  aortic  insufficiency,  with  which  this  con- 
dition may  be  confounded,  is  small  and  weak;  the  blood-pressure  is  prob- 
ably but  little  affected.  Marked  systolic  pulsation  of  the  veins  and  liver 
(positive  venous  pulse)  is  frequently  present,  due  to  the  secondary  tricus- 
pid insufficiency.  In  the  extremities  CEdema  sets  in  readily,  and  there  is 
often  clubbing  of  the  fingers  and  toes  even  in  cases  which  are  not 
congenital. 

The  following  notes  are  taken  from  the  records  of  ihe  medical  service  of  the  Johns 
Hopkins  Hospital: 

Case  of  Pulmonary  Insufficiency. 

R.  R.,  a  colored  laborer,  aged  48,  was  admitted  on  Feb.  8,  1900,  complaining  of 
pain   in  the  stomach  and  chest. 

He  had  measles  and  whooping-cough  as  a  child,  several  attacks  of  tertian  malaria, 
syphilis  in  1897,  rheumatism  in  1899,  and  several  attacks  of  gonorrhoea. 
He  uses  alcohol  and  tobacco  in  moderation. 

Present  illness  began  two  years  ago,  coincident  with  the  onset  of  urethral 
discharge  and  an  attack  of  rheumatism  (gonorrhoeal ?) .  This  caused  him  to 
stop  work.  Since  then  the  rheumatism  has  become  better,  but  he  has  been  troubled  with 
shortness   of   breath   and   palpitation,    though  these  are  not  very  severe. 

Note  by  Dr.  Henry  Harris  states  that  the  patient  is  a  well-nourished  man,  not  dys- 
pnoeic  nor  cyanotic.     Lungs  clear  except  for  a  few  moist  rales  over  the  upper  fronts. 

The  note  on  the  heart  by  Dr.  Osier  on  Feb.  10,  1900,  is  as  follows:  "Chief 
impulse  is  in  the  fourth  left  interspace  just  at  the  nipple,  also  a  little 
impulse  above.  The  impulse  in  the  second  left  interspace  extends  5-6 
cm.  outside  of  the  left  sternal  border.  No  impulse  in  the  aortic  area;  no 
dilated  veins;  no  visible  pulsation  of  the  arteries.  On  palpation  there  is  no 
thrill.  There  is  not  a  very  large  area  of  cardiac  dulness.  The  pulse  is  easily  com- 
pressed and  not  collapsing.  In  the  fifth  interspace,  at  the  apex,  and  over 
the  aortic  area  the  sounds  are  practically  normal.  In  the  fourth  left 
interspace  and  at  the  nipple  itself  both  sounds  are  loud.  There  is  a  short,  distant,  slightly 
rumbling  murmur  before  the  first  sound,  becoming  distinct  on  moving  towards 
the  sternum. 

" At  the  third  interspace  5  cm.  from  the  left  sternal  border  a  short, 
loud  diastolic  murmur  is  heard,  much  louder  as  the  left  sternal  border  is 
approached,  maximal  at  the  left  sternal  border.  There  is  also  a  roughness  of 
the  first  sound.  The  diastolic  murmur  disappears  in  the  sternum,  being  very 
circumscribed.  At  the  second  left  interspace  5  cm.  from  the  left 
.sternal  border  the  diastolic  is  louder.  At  the  left  sternal  border  it  has 
a  maximal  intensity.  There  is  a  short  systolic,  and  a  loud  somewhat  booming  dia- 
stolic, with  a  rough  somewhat  vibratory  quality.  In  the  first  interspace  the  murmur 
diminishes,  being  just  feebly  heard.  In  the  second  interspace  the  murmur  practically 
abolishes  the  second  sound,  which  is  clearly  heard  at  the  aortic  area. 

"No  thrill  after  walking  about.  No  evidence  of  congenital  heart 
disease . 

"The  condition  is  most  likely  pulmonary  insufficiency. 
There  is  a  possibility  of  aneurism,  but  firm  pressure  with  the  stethoscope 
far  out  in  the  second  left  interspace  gives  no  sense  of  lifting  and  no  diastolic 
shock.    There  is  no  tracheal  tugging  and  no  diastolic  shock." 


394  DISEASES   OF   THE    HEART    AND    AORTA. 


DIAGNOSIS. 

The  diagnosis  of  pulmonary  insufficiency  is  rarely  made  during  life. 
The  history  of  very  severe  endocarditis  or  evidence  of  affection  of  several 
valves  or  of  a  lesion  dating  from  birth  leads  to  the  suspicion  of  right-sided 
valvular  disease.  It  is  always  difficult  to  exclude  aortic  insufficiency  or 
the  presence  of  the  two  lesions  at  once.  The  small  size  of  the  pulse, 
the  absence  of  visible  pulsation  of  the  large  arteries,  the  small  pulse-pres- 
sure, the  marked  pulsation  of  the  conus  arteriosus  (both  against  the  chest 
wall  and  as  shown  by  the  fluoroscope) ,  the  retraction  of  the  interspaces 
over  the  right  ventricle,  the  increase  in  the  horizontal  diameter  of  dulness 
to  the  right  and  not  to  the  left,  and  especially  the  dulness  in  the  second 
left  interspace  furnish  the  basis  for  the  diagnosis.  This  is  also  confirmed 
when  there  is  pain  down  the  right  arm  instead  of  the  left.  On  the  other 
hand,  the  congenital  heart  lesions — open  ductus  Botalli,  open  septum 
auriculorum  or  ventriculorum,  etc. — are  very  difficult  to  exclude,  and  will 
be  dealt  with  in  connection  with  congenital  heart  diseases. 

The  diagnosis  of  functional  pulmonary  insufficiency  is  based  upon  the 
presence  of  a  transitory  diastolic  murmur  along  the  left  sternal  border 
during  periods  of  pulmonary  stasis,  in  the  absence  of  other  signs  of  aortic 
insufficiency.  No  doubt  this  diagnosis  may  sometimes  be  made  correctly 
especially  in  cases  of  mitral  stenosis,  but  it  is  one  of  which  even  Gibson 
cannot  feel  certain  in  any  individual  case. 

TREATMENT. 

Treatment  is  the  usual  procedure  for  cardiac  overstrain  of  any  sort, — 
rest,  light  diet,  purgation,  and  digitalis.  Venesection,  by  relieving  the 
distention  of  the  right  auricle  and  ventricle,  is  particularly  useful,  and,  as 
stated  by  Alexander  Morison,  yields  remarkably  good  results  in  this 
condition. 

The  main  hope,  however,  lies  in  bringing  about  the  hypertrophy 
of  the  right  ventricle  and  in  preserving  the  balance  between  the  strength 
of  the  right/  ventricle  and  the  strain  put  upon  it.  Symptomatic  treatment 
of  the  bronchitis  and  pulmonary  complications  may  do  much  to  relieve 
the  patient. 

The  Prognosis  is  bad  when  pulmonary  stenosis  is  present,  but  in  the 
presence  of  a  pure  insufficiency  depends  greatly  upon  the  condition  of  the 
right  ventricles  and  the  amount  of  cardiac  embarrassment  caused  by  the 
lesion.  As  seen  from  Barie's  cases,  patients  may  reach  the  age  of 
seventy-five  in  spite  of  the  lesion.    These  cases  are,  however,  rare. 


BIBLIOGRAPHY. 

Pulmonary  Insufficiency. 

Chevers,  N.:  A  Collection  of  Facts  illustrating  the  Morbid  Conditions  of  the  Pulmonary 

Artery,  Lend.  M.  Gaz.,  1846. 
Frerichs:   Insufficientia  valvularum  arteriae  pulmonae,  Wien.  med.  Wchnschr.,  1853,  iii, 

817  and  833. 


PULMONARY   INSUFFICIENCY.  395 

Benedikt,  J.:  Ein  Fall  von  insufficientia  valvularum  semilunararum  arteriae  pulmonae, 

ibid.,  1854,  iv,  547. 
Walshe:  A  Practical  Treatise  on  Diseases  of  the  Lungs,  Heart,  and  Aorta,  Lond.,  1854. 
Bari6,  E. :  Recherches  sur  I'insuffisance  des  valvules  de  I'artere  pulmonaire.  Arch,  de  med. 

gen.,  Paris,  1891,  i  (vol.  xxvii),  650,  and  1891,  ii  (vol.  xxviii),  30  and  183. 
<jibson,  G.  A.:  Jugular  Reflux  and  Tricuspid  Regurgitation,  Edinb.  M.  J.,  1880,  xxv,  978. 
Preble,  R.  B.:  Relative  Insufficiency  of  the  Pulmonary  Valves,  J.  Am.  M.  Asso.,  Chicago, 

1897,  xxviii,  1012. 
Morison,  A.:  On  Dextral  Valvular  Disease  of  the  Heart,  Edinb.  M.  J.,  1880,  xxv,  102,  439, 

515,  619.  748. 


VII. 
TRICUSPID  IXSUFFICIEXCY. 

ORGANIC    AND    FUNCTIONAL   TRICUSPID    INSUFFICIENCY. 

Insufficiency  of  the  tricuspid  valve  occupies  a  unique  position  among 
the  valvular  lesions.  In  the  functional  form,  due  to  dilatation  of  the  right 
ventricle,  it  is  extremely  common,  and  indeed  probably  occurs  at  some 
stage  in  every  dying  or  failing  heart.  In  the  organic  form,  on  the  other 
hand,  it  is  rare,  occurring  only  16  times  in  1781  cases  of  valvular  disease  at 
the  Johns  Hopkins  Hospital  (0.85  per  cent.)  and  in  less  than  0.7  per  cent, 
of  Gillespie's  cases  at  Edinburgh. 

The  organic  forms  occur  more  frequently  in  severe  or  malignant  endo- 
carditis, as  is  indicated  by  the  fact  that  in  none  of  the  Johns  Hopkins 
cases  was  it  the  only  valve  affected,  mitral  stenosis  being  present  in  10, 
aortic  insufficiency  in  7  of  the  cases.  Three  valves,  the  aortic,  mitral,  and 
tricuspid,  were  involved  in  7  of  these  cases,  the  pulmonary  orifice  once. 
Although  severe  rheumatic  fever  is  perhaps  the  most  frequent  cause, 
streptococcus  and  gonococcus  infections  are  relatively  common  etiological 
factors  (see  Chapter  I),  more  so  than  in  the  milder  valvular  affections. 
Occasionally  it  occurs  as  a  congenital  lesion,  the  result  of  endocarditis 
during  fetal  life. 

Anatomically  the  lesions  of  the  tricuspid  valve  exactly  resemble  those 
of  the  mitral,  with  which  they  are  so  frequently  associated,  being  due  to 
vegetations,  thickenings,  ulcerations,  hemorrhages,  and  occasionally  tumors 
or  malformations  upon  the  valves. 

Functional  Tricuspid  Insufficiency. — Our  knowledge  of  functional  tri- 
cuspid insufficiency  dates  from  the  remarkable  anatomical  and  physiolog- 
ical studies  of  T.  W.  King  in  1837. 

King  stated  that  "  the  right  ventricle  is  liable  to  dilatation  and  that  the  dilatation 
deranges  its  valves. 

"The  last  proposition  is  thus  explained.  The  cavity  is  formed  by  the  solid  septum 
of  the  heart  for  its  inner  wall,  and  by  a  thinner,  more  extensive  and  jielding  layer  of  muscle 
for  its  outer  or  right  wall;  whilst  each  of  these  walls  affords  points  of  attachment  to  the 
cords  of  the  valves.  ...  In  the  progress  of  post-mortem  examinations,  I  have  found  in 
hearts  thus  dilated,  or  only  greatly  distended  by  the  final  congestion,  that  upon  injecting 
the  ventricle  by  the  pulmonary  artery  the  tricuspid  curtains  when  stretched  out  were  under 
all  circumstances  a  great  deal  too  small  to  close  the  opening,  ....  and  it  appears  from 
careful  examination  that  the  united  areas  of  these  vahiilar  portions  are  scarcely  more  than 

equal  to  the  mean  extent  of  the  oval  opening I  have  showTi  that  upon  injecting 

fluids  into  the  ventricles  by  their  respective  arteries  (the  semilunar  valves  destroyed)  the 
left  or  bicuspid  valve  (human  heart)  was  always  seen  to  close  completely  and  firmly,  the 
curtains  being  so  extensive  as  to  fold  together  in  the  form  of  a  cone  or  wedge  within  the 
ventricle,  whilst  the  tricuspid  valve  was  constantly  found  in  its  ordinarj'  state  incapable 
of  preventing  a  considerable  reflux.  With  every  attempt  to  induce  an  accurate  closure 
of  this  valve,  its  scanty  and  divided  curtains  united  imperfectly  or 
scarcely  met,  and  were  only  sufficient  at  the  best  to  form  a  plane 
396 


TRICUSPID   INSUFFICIENCY. 


397 


Fig.  226. — The  outline  of  a  uormal  heart  super- 
posed upon  that  of  a  dilated  heart,  showing  the 
enlargement  of  the  tricuspid  orifice.  Normal  heart 
shown  in  light  shading,  dilatetl  heart  shown  in 
black,  the  diameter  of  the  orifices  in  white  and 
black  bars,  respectively. 


equal    to    the    area    of     the    opening Xo    position    in    or    out 

of  water,  no  degree  of  gentleness  or  force,  no  state  in  anywise 
natural  to  the  organ  that  I  was  able  to  induce,  would  prevent 
a  considerable  riband-like  stream  of  regurgitation  between  the 
ill-apposed  edges  of  the  valve... 
The  only  possible  means  of  obtaining  a  nice, 
though  weak,  adjustment  of  the  tricuspid 
curtains  was  to  compress  the  ventricle,  and 
by  the  same  means  to  lessen  the  extent  of 
the  valvular  aperture.  ...  I  have  twice 
had  an  opportunity  of  experimenting  on  the 
human  heart  at  the  earliest  period  that 
propriety  could  admit  of.  In  one  of  the 
cases  (of  which  I  have  not  hitherto  spoken), 
after  performing  the  experiment  and  eliciting 
results  similar  to  those  related,  the  heart 
was  set  aside,  with  the  expectation  that  its 
tonicity  would  gradually  contract  the 
ventricles  and  fleshy  pillars,  which  accord- 
ingly occurred.  The  first  trial  of  this  heart 
was  made  with  warm  water,  and  the  fluid 
was  thrown  in  at  first  gently,  and  after- 
wards prettj'  forcibly;  but  the  regurgitation 
at  this  time  was  always  considerable.  Now 
upon  repeating  this  experiment  on  the  same 

heart  when  contracted  after  the  lapse  of  a  few  hours,  the  tricuspid  valve  was  still  found 
to  be  much  less  incomplete;  still  in  this  case  there  was  some  refluent  stream.  In  the 
second  case,  however,  under  precisely  similar  circumstances,  I  obtained  at  least  an 
almost  perfect  valvular  action." 

King  also  confirmed  these  observations  by  extended  experiments 
upon  the  hearts  of  a  great  variety  of  mammals  and  birds  during  life  as  well 
as  after  death.  His  experiments  were  repeated  and  substantiated  by  G.  A. 
Gibson  in  1880,  who  showed  that  merely  narrowing  the  orifices  by 
constricting  them  with  a  cord  was  sufficient  to  prevent  the  reflux.  Fran- 
cois-Franck  in  1882  was  able  to  demonstrate  the  production  of  tricuspid 
insufficienc}'  in  the  living  animal  under  conditions  which  led  to  cardiac 
dilatation,  and  to  demonstrate  its  disappearance  under  digitalis.  The 
frequency  with  which  such  functional  insufficiencies  occur  in  heart  failure 
during  life  was  shown  by  Friedreich,  Mahot,  Riegel,  Mackenzie,  Hirsch- 
felder,  and  a  host  of  other  writers.  In  hearts  which  have  been  dilated 
for  a  long  period  there  is  a  considerable  stretching  of  the  valvular  orifice, 
as  was  already  noted  by  King.  This  has  lately  been  very  clearly  shown 
by  Keith's  figures  of  the  hearts  of  Mackenzie's  patients,  in  which  the 
stretching  was  so  great  that  the  usual  narrowing  at  the  auriculoventricular 
opening  had  completely  disappeared  (Fig.  226). 


PATHOLOGICAL    PHYSIOLOGY. 

As  Rosenbach  has  shown,  the  production  of  tricuspid  insufficiency 
has  in  itself  little  effect  upon  the  systemic  circulation.  Blood-pressure 
in  the  arteries  remains  unchanged,  and  there  is  no  characteristic  change 
in  the  pulse.  In  the  pulmonary  circulation  there  may  be  a  slight  fall  of 
pressure  as  a  result  of  the  regurgitation.  On  the  other  hand,  this  may  be 
compensated  b}'  a  slight  increase  in  the  systolic  output  of  the  right  ventricle 
and  no  change  may  occur. 


398 


DISEASES   OF   THE   HEART   AND    AORTA. 


The  principal  effect  of  tricuspid  regurgitation  is 
exerted  upon  the  circulation  in  the  systemic  veins. 
The  blood  thrown  back  into  them  at  each  systole  causes  the  pressure  to 
rise,  so  that  in  such  cases  the  pressure  may  reach  as  high  as  26  cm.  HjO 
(20  mm.  Hg)  (Hooker  and  Eyster).  The  stasis  thus  occurring  also  affects 
the  peripheral  circulation  of  the  limbs  and  body,  giving  rise  to  oedema  and 
ascites;  stasis  in  the  kidneys  causing  diminished  excretion  of  a  concen- 
trated urine  rich  in  albumen  and  casts,  also  stasis  in  the  medulla  oblongata 
where  the  accumulation  of  CO2  causes  a  general  reflex  vasoconstriction. 
The  secondary  effect  of  this  vasoconstriction  is  rise  of  general  blood-pres- 
sure, further  increase  of  the  work  of  the  heart,  and  increased  heart  failure — 
the  vicious  circle  of  asphyxia  (see  page  27). 


NORMAL 


TRICUSPID 
INSUFFICIENCY 


AO 

AO 

MAX    ^ 

MAX 
_MIN. 

K 

MIN     I^H 

\ 

^ 

\ 

\   ^ 

y  ^A 

V  r^- 

^Ji^^^-^LA 

v/ 

1         "t          vi    1 

1^ 

RA 

1 

i 

>a^ 

^ 
\ 

^ 

r 

H 

LA 

1 

Fig.  227. — Diagram  showing  the  changes  in  the  circulation  in  tricuspid  insuflBciency.  The  arrows 
show  the  rise  in  pressure  in  the  right  auricle  {RA )  and  vena  cava,  and  the  fall  of  pressure  in  the  pulmonary 
artery  (PA).  The  white  curves  represent  the  pulse-waves,  that  above  RA  showing  the  ventricular  type 
of  the  venotis  pulse. 


Venous  Pulse  in  Tricuspid  Insufficiency. — In  contrast  to  the  normal 
(negative,  presystolic,  diastolic,  "double")  venous  pulse,  the  typical  pulsa- 
tion in  tricuspid  insufficiency  is  synchronous  with  and  of  the  same  frequency 
as  ventricular  systole  (single  venous  pulse)  (Friedreich,  Riegel,  Mackenzie, 
Hirschf elder) .  Since  there  is  a  free  communication  between  auricle  and 
ventricle,  the  jugular  pulse-wave  (Fig.  228)  closely  resem- 
bles the  curve  of  intraventricular  pressure,  with  its 
up-stroke  and  plateau  during  systole  and  its  fall  during  diastole.  In  the 
advanced  stages  the  wave  (a)  due  to  auricular  systole  is  absent,  since  the 
auricles  are  paralyzed  (Mackenzie). 

Mackenzie  states,  however,  that,  contrary  to  preconceived  notions, 
all  cases  with  tricuspid  insufficiency  do  not  necessarily  show  a  positive 
venous  pulse,  and  in  a  number  of  his  Cases  which  at  autopsy  showed  both 
organic  and  functional  insufficiencies  the  positive  venous  pulse  was  absent. 
Mackenzie  finds  in  these  cases  that  the  up-stroke  of  the  wave  (r),  which  is 
due  to  stagnation  in  the  ventricle,  begins  earlier  than  usual.  As  the  lesion 
increases,  this  wave  (reflux)  begins  sooner  and  sooner  after  the  beginning 
of  systole,  until  finally  it  takes  up  the  entire  systolic  period,  and  the  posi- 


TRICUSPID   INSUFFICIENCY. 


399 


JUG. 


BRACH. 


tive  or  ventricular  type  is  assumed.  These  observations  have  been  con- 
firmed in  man  by  Gibson  and  Sewall,  and  in  animals  with  tricuspid  lesions 
by  J.  Rihl,  who  found  that  as  long  as  the  regurgitation  was  slight  the 
auricular  type  of  venous  pulse  persisted,  but  when  it  became  severe  this 
gave  way  to  the  ventricular  type.  As  Sewall  states,  "  among  patients  pre- 
senting themselves  for  examination  on  account  of  a  wide  range  of  func- 
tional disorders,  I  have  been 
struck  with  the  uniformity 
with  which  evidences  of  cardiac 
insufficiency  could  be  distin- 
guished, based  upon  the  nature 
of  the  symptoms  and  the  char- 
acter of  the  venous  pulse  .  .  . 
The  V  wave  has  a  double  crest; 
or  rather,  the  wave  v,  which 
begins  just  at  the  moment  of 
closure  of  the  aortic  valves,  as 
determined  by  the  dicrotic 
notch  in  the  lower  tracing,  is 
immediately  preceded  by  a  wave 
which  is  completed  during  the 
last  moments  of  ventricular 
outflow."  He  believes  that 
this  last-mentioned  wave  (the 
t  wave  of  Bard)  is  produced  by 
a  slight  regurgitation  due  to 
weakness  of  the  papillary  mus- 
cles, and  is  indicative  of  such 

regurgitation,  but  he  does  not  take  into  account  the  fact  that  it  may 
be  present  without  any  other  signs  of  tricuspid  insufficiency.  On  the  other 
hand,  as  shown  by  Theopold,  Hewlett,  and  others  (page  75),  the  positive 
venous  pulse  may  be  present  without  any  regurgitation  at  the  tricuspid. 


r\/\ 

c            c 

-A 

c 

J  1 

\    K 

^ 

w 

c             c 

c 

,'       V 

1  /  ^ 
.  c 

;SEC. 


Fig.  228. — Venous  pulse  of  patients  with  tricuspid 
insufficiency  (positive  venous  pulse).  JUG.,  pulsation 
over  the  jugular  vein;  BRACH.,  pulse  in  the  brachial 
artery;  c,  moment  of  onset  of  the  pulse-wave  in  the 
carotid  artery.  The  tracing  shows  an  elevation  through- 
out systole,  with  a  very  slight  depression  (perhaps  due  to 
fling)  immediately  following  the  upstroke.  The  curve 
corresponds  almost  exactly  to  the  curve  of  pressure  in 
the  right  ventricle. 


Fig.  229. —  Venous  pulse  of  another  patient.  VJD,  right  jugular  pulse;  ACS,  left  carotid  artery. 
The  slow  slanting  upstroke  indicates  a  slightly  less  smaller  leak  than  in  the  preceding  case.  There  is  no 
fling,  and  hence  no  midsystolic  depression. 


SYMPTOMS. 


The  condition  of  patients  with  tricuspid  insufficiency  well  illustrates 
the  fact  that  this  is  one  lesion  which  is  not  often  compensated,  though  com- 
pensation can  take  place  through  increased  suction-pump  action  of  the 
right  ventricle.  They  are  usually  markedly  dyspnoeic  or  orthopnoeic,  weak 
and  readily  exhausted  by  the  slightest  effort,  often  drowsy  and  somnolent. 


400  DISEASES   OF   THE    HEART    AND    AORTA. 

Palpitation  may  be  extreme.  One  of  the  early  symptoms  is  pain  in  the 
region  of  the  liver,  from  the  stretching  of  the  capsule.  This  is  often  accom- 
panied by  slight  jaundice;  and  the  appearance  of  an  icteroid  hue  is  one  of 
the  unfavorable  signs  in  tricuspid  insufficiency,  since  it  marks  an  intense 
hepatic  stasis.  Gastric  disturbances,  loss  of  appetite,  and  indigestion  are 
the  rule  and  vomiting  is  frequent. 

PHYSICAL    EXAMINATION. 

The  patients  are  usually  quite  pale  and  deeply  cyanotic.  When 
secondary  renal  changes  have  set  in,  the  face  may  be  puffy.  Emaciation 
and  slight  jaundice,  the  result  of  catarrhal  cholangitis  from  stasis  in  the 
portal  system,  are  among  the  most  suggestiv^e  signs  that  tell  the  onset  of 
tricuspid  insufficiency.  The  veins  are  full  and  show  well-marked  pulsation, 
systolic  in  time  and  synchronous  with  the  carotid  pulse.  There  is  often 
oedema  of  the  extremities,  genitalia,  and  back,  and  large  ecchymoses  are 
not  uncommon.  Ascites  and  right-sided  hydrothorax  are  seen  in  the  last 
stages  of  almost  every  case.  Examination  of  the  eye-grounds  usualh'  shows 
distention  of  the  retinal  veins  (Black).  The  urine  is  usually  scant  and 
concentrated,  and  contains  a  large  amount  of  albumen  and  casts  in  large 
numbers. 

Heart. — The  precordium  often  bulges,  and  the  very  vigorous  beating 
of  the  hypertrophied  right  ventricle  is  seen  in  the  retraction  of  the  inter- 
spaces between  the  parasternal  line  and  sternal  margin.  In  the  epigastrium 
and  over  the  liver  a  systole  pulsation  is  seen  and  felt.  Percussion 
shows  a  marked  extension  of  the  cardiac  dulness  to  the  right  of  the  sternum, 
due  to  dilatation  of  the  right  ventricle.  It  often  reaches  5-6  cm.  from  the 
midline,  but  the  cardiohepatic  angle  remains  acute.  There  may  be  or  may 
not  be  extension  of  dulness  to  the  left  mammillary  line,  dependent  upon 
the  presence  of  weakness  of  the  left  ventricle.  The  characteristic  modifi- 
cation of  the  heart  sounds  is  the  presence  of  a  s  y  s  t  o  1  i  c  murmur 
which  is  over  and  near  the  lower  third  of  the  sternum,  but  may  also  be 
heard  over  the  greater  part  of  the  heart,  over  the  ensiform  cartilage,  and  in 
the  epigastrium.  It  is  loudest  in  the  fourth  and  fifth  right  interspaces, 
between  the  parasternal  and  the  midline.  Occasionally,  as  in  Case  J.  D.,  this 
murmur  cannot  be  heard  when  the  patient  is  lying  on  his  back  or  even 
standing,  but  can  be  elicited  by  causing  him  to  bend  forward  to  an  angle 
of  45°.  This  does  not  increase  the  accidental  murmur  which  is  often  heard 
over  the  entire  right  ventricle,  nor  does  it  augment  cardiopulmonary  mur- 
murs over  this  area. 

The  murmur  is  often  accompanied  by  a  systolic  thrill  over  the  lower 
sternum  and  neighboring  portions  of  the  chest  wall.  The  distribution  to 
the  right  of  and  behind  the  sternum  corresponds  to  the  wall  of  the  right 
auricle,  the  chamber  into  which  the  regurgitant  stream  is  conducted  (see 
Figs.  230  and  231).  The  area  to  the  left  of  the  sternum  over  which  the 
murmur  is  loudly  heard  corresponds  to  the  wall  of  the  right  ventricle.  As 
in  mitral  insufficiency,  it  is  difficult  to  explain  the  loud  transmission  of  this 
murmur  in  a  direction  opposite  to  that  of  the  leakage,  but  it  seems  possible 
that  the  vibrations  of  the  valve  may  be  communicated  to  the  ventricular 
wall  along  the  tense  chordae  tendineae.    The  murmur  is  rarely  transmitted 


TRICUSPID   INSUFFICIENCY. 


401 


Fig.  230,  :  .  -:  .  rion  of  the  iminnur  aivl  rai'iiiac 
outline  in  tricuspid  insufficiency.  The  shaded  area  indi- 
cates the  region  over  which  the  systolic  murmur  is  heard, 
the  diagram  at  the  left  indicates  its  relation  to  the  cardiac 
cycle.  The  heart  is  seen  to  be  enlarged  to  the  right.  The 
systolic  pulsation  of  the  liver  is  indicated  by  the  small 
diagram  and  the  arrows. 


as  far  as  the  pulmonary  area,  though  a  systolic  murmur  of  different  origin 
(accidental  murmur)  is  often  heard  in  the  latter  area  in  cases  with  tricuspid 
insufficiency  as  well  as  in  others.  The  tricuspid  murmur  is,  as  a  rule,  not 
transmitted  to  the  apex.  Most  frequently  in  dilated  hearts  there  is  also  a 
functional  mitral  insufficiency 
coexisting,  and  it  is  this  which 
gives  rise  to  a  systolic  murmur 
at  the  apex  and  in  the  axilla,  but 
this  is  usually  less  superficial 
than  the  tricuspid  murmur  and 
it  can  usually  be  differentiated 
from  the  latter.  Moreover,  there 
is,  between  the  two  areas  at 
which  each  murmur  has  its 
maximum,  a  zone,  correspond- 
ing to  the  interventricular  sep- 
tum, at  which  both  murmurs 
diminish  in  intensity. 

As  Hering  and  others  have 
shown,  a  systolic  murmur  is 
not  heard  in  all  cases  of  tricus- 
pid insufficiency,  especially  in 
those  in  which  the  heart  is  too 
weak  to  give  rise  to  a  loud 
sound  or  in  which  the  aperture 

of  leakage  is  too  loud  to  produce  one  (large  leaks).  Sometimes  the  murmur 
has  a  musical  character.  Occasionally,  as  in  Case  W.  H.,  in  which  the  pres- 
ence of  tricuspid  insufficiency  was  demonstrated  conclusively  by  venous 
and  liver  tracings  during  life  and  by  autopsy,  peculiar  diastolic  murmurs 

are  heard  over  the  right  ventricle, 
especially  along  the  left  sternal  mar- 
gin. They  are  sometimes  blowing  and 
sometimes  rumbling  (mid-diastolic  in 
character),  and  may  perhaps  be  caused 
by  functional  insufficiency  of  the  pul- 
monic valves  due  to  the  dilatation  of 
the  right  ventricle. 

Organic  murmurs  are  frequently 
rough,  while  those  due  to  functional 
insufficiency  are  usually  soft  and  blow- 
ing, and  sometimes  barely  audible. 
Hering  states,  as  the  result  of  pro- 
longed experimental  investigation, 
that  functional  insufficiency  which  gives  rise  to  distinct  murmurs  is 
usually  of  slight  grade,  but  when  the  orifice  is  much  dilated  and  the  leak 
is  a  large  one  no  murmur  is  heard.  This  aphony  of  the  valves  corre- 
sponds to  the  condition  described  on  page  110. 

Except  for  the  accompanying  murmur  which  often  replaces  the  first 
sound,  the  cardiac  sounds  are  not  greatly  modified.     The  sounds  at  the 
26 


Fig.  231. — Cross  section  of  the  body,  show- 
ing the  paths  of  propagation  of  the  munnur  of 
tricuspid  insufficiency. 


402  DISEASES   OF   THE   HEART    AND    AORTA. 

base  are  very  considerably  dependent  upon  the  pulmonary  and  aortic  pres- 
sures and  on  the  degree  of  arteriosclerosis,  and  hence  their  relative  loudness 
varies  considerably. 

Pulse. — The  radial  pulse  in  tricuspid  insufficiency  is  usually  small  and 
weak  and  often  irregular.  The  arrhythmia  usually  assumes  the  character 
of  permanent  absolute  irregularity  (pulsus  irregularis  perpetuus)  (see  page 
75)  and  is  accompanied  by  paralysis  of  the  auricles. 

Blood=pressure. — The  blood-pressure  is  usually  normal  or  a  little  below 
normal;  but  there  are  no  characteristic  features,  and  secondary  rises  of 
blood-pressure  from  medullary  asphyxia  are  common. 

The  liver  is  usually  enlarged  and  may  extend  far  below  the  costal 
margin  or  even  below  the  umbilicus.  It  is  usually  hard  and  its  edge  smooth, 
and  often  shows  a  distinct  systolic  pulsation  (Fig.  232). 

I  II 

SYSTOLIC   PULSATION  SYSTOLIC   RETRACTION 


Fig.  232. — ^Tracings  of  liver  pulsation.  I.  Systolic  pulsation  of  the  liver  in  tricuspid  insufBciency. 
LIV,  tracing  from  the  liver;  BRACH,  tracing  from  the  brachial  artery;  h,  pulse-wave  in  the  brachial  ar- 
tery; c  and  d  have  their  usual  significance.  The  upstroke  of  the  arrow  indicates  a  protrusion,  the  downstroke 
a  retraction.  II.  Systolic  retraction  over  the  liver  from  a  case  of  marked  hypertrophy  of  the  right  heart. 
CAR,  tracing  from  the  carotid  artery. 

Ascites  and  oedema  of  varying  grades  may  be  but  are  not 
always  present,  dependent  upon  the  patient's  condition.  "  Broken  com- 
pensation" does  not  always  indicate  "tricuspid  insufficiency,"  nor  vice 
versa. 

CASES  OF  TRICUSPID  INSUFFICIENCY. 

Myocarditis  with  Tricuspid  Insufficiency  and  probably  also  Pulmonary 

Insufficiency. 

W.  H.,  colored  driver,  aged  48,  first  admitted  to  the  Johns  Hopkins  Hospital  on  May 
12,  1896,  complaining  of  swelling  of  the  feet  and  shortness  of  breath.  He 
had  always  been  healthy  except  for  measles  and  chicken-pox  in  childhood  and  malaria  in 
1861.    Gonorrhoea  at  33  but  no  lues.    Drinks  and  smokes  in  moderation. 

Present  illness  began  during  the  past  winter,  with  gradually  developing  shortness 
of  breath,  especially  on  exertion.  After  such  attacks  the  extremities  would  swell  very 
much.    A  few  days  before  admission  his  testicle  also  began  to  swell. 

On  examination  by  Dr.  Thayer  at  this  time  he  was  found  to  be  a  well-formed  colored 
man,  mucous  membranes  of  good  color.  Lungs  clear  except  for  moist  rales  over  the  right 
front.  The  apex  was  then  in  the  sixth  interspace  at  the  m  a  m  m  i  1 1  a  r  y 
line.  The  first  sound  was  feeble,  but  no  murmurs  were  heard.  The  abdomen  was  full; 
liver  and  spleen  not  palpable.  SUght  oedema  of  the  extremities.  The  oedema  dis- 
appeared under  rest  and  digitalis.  The  patient  gained  in  strength  and  was  discharged  in 
three  weeks.  He  returned  again  three  years  later,  with  similar  s>-mptoms,  and  again 
made  a  rapid  recovery.  On  this  admission  the  liver  was  felt  by  Dr.  McCrae. 
He  was  treated  in  the  hospital  repeatedly  during  the  next  few  years,  always  presenting 


TRICUSPID   INSUFFICIENCY.  403 

about  the  same  clinical  picture.  On  Dec.  9,  1903,  the  apex  was  14.5  cm.  to  the 
left  of  the  midline,  and  Dr.  Thayer  noted  that  the  sounds  were  clear  in  the  tricuspid  area. 
There  was,  however,  a  soft  diastolic  and  a  rumbling  presystolic  murmur 
heard  over  the  heart  between  the  left  parasternal  line  and  the  sternal  margin  (pulmonary 
insufficiency).  When  he  first  came  under  the  writer's  care  in  July,  1904,  during  a  similar 
attack  of  cardiac  failure,  this  diastolic  murmur,  and  indeed  all  the  other  murmurs, 
had  disappeared,  the  heart  sounds  were  very  feeble  and  the  heart  action 
irregular.  As  his  condition  improved  under  treatment,  the  former  murmur 
reappeared  and  increased  to  about  the 
previous  intensity,  though  heard  only  with  the 
larger  beats.  During  the  next  admission  a  few 
months  later  the  rumble  was  definitely  mid-dias- 
tolic  and  very  rough. 

Blood-pressure  during  these  admissions 
ranged  from  130  to  160  mm.  Hg. 

He  was  readmitted  for  the  last  time  in 
October,  1905,  the  sounds  being  about  as  before, 
the  oedema  somewhat  greater.     There  was  severe  ^^^  233.-Systolic  pulsation  of  the  liver 

nght-sided    hydrothorax.       Venous      of   patient  W.  H.     Cor.,  carotid  arterial 
tracings    showed    a    positive    venous    pulse    of       pulse;  s,  onset  of  ventricular  systole. 
the     ventricular     type,     and     there     was 

systolic  pulsation  of  the  liver  (tricuspid  insufficiency)  (Fig.  233). 
The  blood-pressure  during  this  admission  was  110  mm.,  but  rose  to  130 
mm.    on   the   day  before   death. 

Autopsy  showed  dilatation  of  the  right  auricle  and  ventricle, 
dilatation  of  the  pulmonary  artery,  marked  sclerosis  of  the  cor- 
onary arteries,  very  marked  chronic  fibrous  myocarditis  (cardiosclerosis), 
and  relative  tricuspid  insufficiency.  There  was  marked  cardiac  hyper- 
trophy, the  heart  weighing  620  Gm.  There  were  also  chronic  passive  congestion  of  the 
viscera,  cirrhosis  of  the  liver,  chronic  interstitial  nephritis,  chronic  fibrous  pleurisy,  and 
acute  gastritis.  There  were  no  valvular  lesions  and  there  was  no  tricuspid  steno- 
sis to  account  for  the  middiastolic  rumble.  It  is  quite  probable  that  there  was  during  life 
a  functional   pulmonary  insufficiency. 

Case  of  Mitral  and  Tricuspid  Insufficiency. 

J.  D.,  painter,  aged  69,  came  to  Johns  Hopkins  Dispensary  complaining  of  swell- 
ing of  the  limbs.  He  has  always  been  healthy  except  for  inflammatory  rheu- 
matism off  and  on  during  the  last  twenty  years.  Denies  venereal  disease.  Has  not 
worked  during  the  past  twenty  years. 

He  has  had  swelling  of  the  feet  and  legs  after  exertion  during  the  past  four  years, 
some  shortness  of  breath,  but  can  always  sleep  without  a  pillow.  His  legs 
and  penis   have   been   swollen   for   the   past   month. 

The  patient  is  a  well-nourished  man,  looking  much  younger  than  he  acutally  is. 
His  color  is  a  trifle  sallow  but  not  icteroid.  Pupils  equal.  No  glandular  enlargement. 
No  lead  line  on  the  gums,  in  spite  of  his  occupation.  The  chest  is  clear  on  percussion 
and  auscultation  except  for  a  few  wheezing  rales  at  the  bases. 

The  heart  is  markedly  enlarged,  d  u  1  n  e  s  s  extending  to  the  anterior  ax- 
il 1  ar  y  line  in  the  fifth  left  interspace,  above  to  the  middle  of  the  second  left  interspace 
and  5  cm.  to  the  right  of  the  midline.  At  the  apex  the  first  sound  ip 
replaced  by  a  blowing  systolic  murmur  heard  distinctly  throughout  the  entire 
left  axilla,  this  diminishes  in  intensity  to  the  right  of  the  mammillary  line.  When  the 
patient  is  standing  and  bending  forward  at  an  angle  of  45°,  a  loud 
blowing  systolic  murmur  of  different  character  is  heard  over  the  entire  tri- 
cuspid area,  but  this  is  not  evident  in  any  other  position.  In  the  pulmonic  area 
there  is  a  loud  blowing  mesosystolic  murmur,  also  heard  in  the  second  right  interspace, 
but  not  transmitted  to  the  carotid  arteries.  The  heart's  action  is  somewhat  irregular; 
the  jugular  veins  are  distended  but  do  not  pulsate;  the  venous  pressure,  as  shown 
by  Gaertner's  method,  is  high.  (The  veins  of  the  back  of  the  hand  and  wrist 
do  not  empty  until  the  hand  is  about  20  cm.  above  the  level  of  the  heart.) 


404  DISEASES   OF  THE   HEART   AND   AORTA. 

The  liver  is  not  palpable.  There  is  little  if  any  fluid  in  the  abdominal  cavity.  The 
scrotum  and  penis  are  markedly  csdematous,  as  are  also  the  legs  and  thighs. 

The  patient  entered  the  hospital,  where  he  died  of  heart  failure  a  few  days  later. 

DIAGNOSIS. 

The  absolute  diagnosis  of  tricuspid  insufficiency  depends  upon  the 
presence  of  a  dilatation  of  the  right  auricle  (increased  dulness  to  the  right), 
a  systolic  murmur  loudest  at  and  about  the  base  of  the  sternum,  a  positive 
venous  pulse  of  the  ventricular  type,  and  an  enlarged  liver  with  systolic 
pulsation. 

As  has  been  seen  above,  these  features  are  not  always  present.  Hering  has  summed 
up  the  whole  question  in  the  following  conclusions: 

1.  A  large  tricuspid  insufficiency  may  give  no  murmur,  but  small  regurgitations 
usually  give  distinct  murmurs. 

2.  A  small  tricuspid  regurgitation  may  cause  no  change  in  the  venous  pulse,  but  a 
large  leakage  gives  rise  to  a  positive  venous  pulse  of  the  ventricular  type.    Hence, 

I.  Loud  murmur  +  auricular  (presystolic,  diastolic,  double,  physiological)  venous 
pulse  =  slight  tricuspid  regurgitation. 

II.  No  murmur  +  positive  ventricular  venous  pulse  +  systolic  pulsation  of  hver  = 
severe  tricuspid  regurgitation. 

TREATMENT. 

Frangois-Franck  showed,  in  his  experiments  upon  functional  tricuspid 
insufficiency,  that  the  administration  of  digitalis  caused  the  signs  of  insuffi- 
ciency to  disappear.  This  is  in  perfect  harmony  with  the  clinical  experience 
that  "broken  compensation"  (and  tricuspid  insufficiency)  is  in  general 
the  signal  for  digitalis,  and  the  administration  of  this  drug  furnishes  the 
main  therapeutic  measure.  Absolute  rest  is  necessary  for  prolonged  periods; 
but  after  the  tricuspid  insufficiency  has  persisted  for  months  in  spite  of  it, 
it  is  useless  to  reduce  the  patient  to  a  permanently  bedridden  condition 
in  the  hope  of  final  recovery.  It  is  better  to  render  his  life  as  pleasant  as 
possible  under  the  conditions,  to  let  him  sit  up  and  move  quietly  about  the 
house,  go  driving,  or  indulge  in  other  pleasant  diversions  which  do  not 
entail  exercise,  effort,  or  excitement.  It  must  not  be  forgotten  that  worry 
and  nervousness  bring  on  palpitation  and  cardiac  overstrain  almost  as 
readily  as  does  exercise;  and,  conversely,  mental  diversion  and  cheerfulness 
assist  in  re-establishing  conditions  favorable  for  cardiac  recovery.  The 
important  feature  in  this  phase  in  the  management  of  the  case  is  the  avoid- 
ance of  dyspnoea.  The  simple  methods  of  counting  between  steps  on  a 
staircase  or  of  taking  for  one's  gait  one  step  for  each  inspiration  may  give 
the  patient  considerable  latitude  for  accomplishment  without  strain  or 
injury. 

Diet  should  always  be  light,  partly  to  avoid  the  strain  on  the  heart, 
partly  on  account  of  the  disordered  digestion,  gastritis,  and  catarrhal 
jaundice,  which  are  entailed  by  portal  stasis. 

The  bowels  should  be  kept  open  with  saline  purgatives  and  several 
movements  a  day  should  be  secured. 

In  stages  of  acute  heart  failure  when  the  venous  pressure  is  high  and 
the  right  auricle  much  distended,  venesection  should  be  resorted 
to  promptly  and  continued  until  the  right  border  of  the  heart  has  receded. 


TRICUSPID   INSUFFICIENCY.  405 

The  best  results  are  obtained  when  venesection  is  accompanied  by  intra- 
venous injection  of  strophanthin  (^  mg.)  (see  page  177)  and  this  followed 
by  free  purgation  and  digitalis. 

BIBLIOGRAPHY. 
Tricuspid  Insufficiency. 

Gillespie,  A.  L.:  An  Analysis  of  2368  Cases  admitted  with  Cardiac  Lesions  into  the  Royal 

Infirmary,  Edinburgh,  Edinb.  Hosp.  Rep.,  1897,  v,  31. 
King,  T.  W.:  An  Essay  on  the  Safety-valve  Function  in  the  Right  Ventricle  of  the  Human 

Heart,  Guy's  Hosp.  Rep.,  Lond.,  1837,  ii,  104.    Part  II.  On  the  Safety-valve  Action 

in  the  Mammalia,  ibid.,  142.    Part  III.  Of  the  Safety-valve  in  Birds,  ibid. 
Gibson,  G.  A.:  Jugular  Reflux  and  Tricuspid  Regurgitation,  Edinb.  M.  J.,  1880,  xxv,  979. 
Fran^ois-Franck :  Sur  la  part  importante  qui  revient  a  I'etat  du  muscle  cardiaque  dans  la 

production   des   insuffisances   tricuspidiennes   transitoires,   Compt.-rend.   Soc.   Biol., 

Paris,  1882,  xxxiv,  88. 
Friedreich,  N.:  Ueber  den  Venenpuls,  Deutsch.  Arch.  f.  klin.  Med.,  Leipz.,  1866,  i,  241. 
Mahot:  Des  battements  du  foie  dans  I'insuffisance  tricuspide,  These,  Paris,  1869. 
Riegel,  F.:  Ueber  den  normalen  und  pathologischen  Venenpuls,  Deutsch.  Arch.  f.  klin. 

Med.,  1882,  xxxi,  26. 
Mackenzie,  J.:  The  Venous  and  Liver  Pulses,  and  Arrhythmic  Contractions  of  the  Cardiac 

Cavities,  J.  Path,  and  Bacteriol.,  Edinb.  and  Lond.,  1894,  ii,  84,  273.    The  Study  of 

the  Pulse  and  Movements  of  the  Heart,  Lond.,  1903.    The  Interpretation  of  Pulsa- 
tions in  the  Jugular  Veins,  Am.  J.  M.  Sci.,  Phila.,  1907,  cxxxiv,  12. 
Hirschfelder,  A.  D.:  Graphic  Methods  in  the  Study  of  Cardiac  Diseases,  ibid.,  1906,  cxxxii, 

378.     Inspection  of  the  Jugular  Vein;    its  Value  and  its  Limitations  in  Functional 

Diagnosis,  J.  Am.  M.  Asso.,  Chicago,  1907,  xlviii,  1105. 
Keith,  A.:  An  Account  of  the  Structures  concerned  in  the  Production  of  the  Jugular  Pulse, 

J.  Anat.  and  Physiol.,  Lond.,  1907,  xliii,  1. 
Rosenbach,  O.:  Ueber  artifizielle  Herzklappenfehlern,  Arch.  f.  exper.  Path.  u.  Pharmakol., 

Leipz.,  1878,  ix,  1. 
Hooker,  D.  R.,  and  Eyster,  J.  A.  E.:  An  Instrument  for  the  Determination  of  Venous. 

Blood-pressure  in  Man,  Bull.  J.  Hopkins  Hosp.,  Balto.,  1908,  xix,  274. 
Gibson,  G.  A.:  Our  Debt  to  Ireland  in  the  Study  of  the  Circulation,  Reprint  from  the 

Dublin  J.  M.  Sci.,  1907. 
Rihl,  J.:  Ueber  den  Venenpuls  nach  experimenteller  Lasion  der  Trikuspidalklappe,  Ver- 

handl.  d.  Kong.  f.  innere  Med.,  Wiesbaden,  1907,  xxiv. 
Sewall,  H.:  Safeguards  of  the  Heart-beat,  Am.  J.  M.  Sci.,  Phila.,  1908,  cxxxvi,  32. 
Hering,  H.  E.:  Ueber  pulsus  irregularis  perpetuus,  Deutsch.  Arch.  f.  klin.  Med.,  Leipz., 

1908,  xciv,  185. 


VIII. 
TRICUSPID  STENOSIS. 

OCCURRENCE    AND    ETIOLOGY. 

Stenosis  of  the  tricuspid  orifice  belongs  to  the  rarer  valvular  lesions, 
and  also  to  the  group  which  rarely  occurs  alone.  In  the  24,000  cases  which 
have  been  admitted  to  the  Medical  Service  of  the  Johns  Hopkins  Hospital 
tricuspid  stenosis  has  been  found  in  only  seven  cases,  in  all  of  which  other 
lesions  were  present.  W.  W.  Herrick  has  recently  given  the  following 
statistics  from  187  cases  collected  from  the  literature: 

Summary  of  Reported  Cases. 

Sex. 

Male 38 

Female 13.3 

Sex  not  known 16 

Age. 

10  to  20  years 16 

20  to  30  years 59 

30  to  40  years 38 

40  to  50  years 28 

50  to  60  years 10 

60  to  70  years 6 

Not  known 30 

187 

Previotts  History. 

Rheumatism 61 

Doubtful  rheumatism  or  chorea 11 

No  rheumatism 33 

Not  known 82 

Association  of  Valvular  Lesions. 

Tricuspid  alone 14 

Tricuspid  and  mitral 102 

Tricuspid  and  aortic 64 

Tricuspid  and  aortic  and  pulmonary 1 

Tricuspid  and  endocardium  of  left  auricle 1 

Tricuspid,  mitral,  and  pulmonary 2 

Total  cases 184 

Cases  showing  adherent  pericardium 12 

In  Leudet's  series  rheumatism  was  an  etiological  factor  in  over  50  per 
cent.,  puerperal  fever  in  5  per  cent.  Syphilis  has  also  been  assigned  as  a 
causal  factor. 

406 


•    TRICUSPID   STENOSIS.  407 

In  the  cases  in  which  the  tricuspid  stenosis  follows  the  mitral  stenosis 
the  same  etiological  factors  are  concerned  as  for  the  single  lesion.  In  view 
of  the  work  of  Goodhart,  Roy  and  Adami,  and  Weber  and  Deguy  quoted 
above  (page  359) ,  it  is  not  unlikely  that  the  overstrain  of  the  right  ventricle, 
brought  about  by  the  latter  conditions,  leads  to  oedema  and  hemorrhage 
into  the  tricuspid  valve,  and  that  these  processes  usher  in  the  fibrosis.  In 
other  words,  the  mitral  stenosis  itself  becomes  an  etiological  factor  in  the 
tricuspid  lesion,  and  the  pathological  process  completed  in  the  mitral  is 
now  transferred  back  one  step  in  the  circulation  and  repeats  itself  in  the 
tricuspid. 

Occasionally,  as  in  a  case  reported  by  Gairdner,  a  fibrinous  ball,  a 
tumor,  or  a  hemorrhage  into  the  valve  may  assist  in  producing  the  stenosis. 

A  certain  percentage  of  the  cases  are  congenital  in  origin. 

PATHOLOGICAL    ANATOMY. 

The  anatomical  changes  in  the  valve  are  exactly  similar  to  those 
which  occur  upon  the  mitral  in  stenosis  of  that  orifice :  a  progressive  fibro- 
sis accompanied  by  fusion  of  the  cusps  along  their  line  of  closure,  and 
gradual  web-like  extension  of  the  valvular  membrane,  which  grows  down- 
ward between  the  shrunken  chordae  tendinese  forming  an  elongated  funnel 
with  narrow  outlet. 

The  liver  is  usually  enlarged,  though  in  some  cases  it  may  be  smaller 
than  usual,  owing  to  the  cirrhotic  changes  and  perihepatitis  which  result 
from  the  prolonged  stasis. 

PATHOLOGICAL    PHYSIOLOGY. 

The  changes  which  tricuspid  stenosis  produces  are  exactly  similar 
to  those  already  seen  in  mitral  stenosis,  except  that  they  affect  the  systemic 
veins  instead  of  the  pulmonic.  The  filling  of  the  right 
ventricle  is  retarded.  The  amount  of  blood  which  enters  it 
passively  in  early  diastole  is  diminished,  and  the  amount  driven  in  by  the 
auricle  is  increased.  The  auricle  thus  begins  to  hypertrophy.'  Its  strength 
increases,  and  the  presystolic  wave  which  it  produces  in  the  venous  pulse 
increases  in  size.  In  well-marked  cases  the  force  of  auricular  contraction 
may  be  great  enough  to  produce  a  definite  presystolic  pulsation  in  the 
liver  with  a  wave  exactly  similar  to  that  found  in  the  vein  (Mackenzie). 

When  the  tricuspid  orifice  is  narrowed  to  such  an  extent  that  the 
increased  force  of  the  auricle  no  longer  empties  the  latter,  the  auricular 
contraction  begins  to  drive  the  blood  back  into  the  veins  and  to  increase 
the  already  high  venous  pressure,  thus  still  further  impeding  the  circula- 
tion through  the  heart  and  lungs,  so  that  the  aeration  of  the  blood  is  greatly 
interfered  with  and  marked  cyanosis  produced.  This  in  turn  gradually 
predisposes  to  polycythaemia  (red  blood  count  8,000,000  to  9,000,000). 
The  latter  condition  causes  increased  viscosity  of  the  blood,  and  still 
further  increases  the  burden  upon  the  heart.     On  the  other  hand,  the 

'  The  right  ventricle  is  almost  always  hypertrophied  in  tricuspid  stenosis,  owing  to 
the  presence  of  mitral  stenosis  and  tricuspid  insufficiency. 


408 


DISEASES   OF   THE   HEART   AND    AORTA. 


hypertrophy  of  the  right  auricle  gradually  reaches  its  limit,  and  when 
the  venous  pressure  becomes  too  high  from  exercise  or 
other  cause,  this  chamber  becomes  dilated  and  paralyzed,  and  the  pre- 
systolic wave  disappears  from  the  jugular  and  liver  pulse  (Mackenzie). 
Unlike  lesions  of  other  valves,  no  further  compensation  is  now 
possible,    and  only  rest  of  the  heart  can  prevent  the  over-distention  of 

the  veins.    Consequently  slight 
NORMAL  :  TRICUSPID  STENOSIS        overstrain   results    at  once   in 

venous  stasis,  cedema,  etc., 
which  may  pass  off  readily 
when  the  patient  is  at  rest. 

The  liver  is  often,  though 
not  always,  enlarged;  and  a 
pulsation  presystolic  in  time 
may  be  felt  in  it  as  long  as 
the  right  auricle  is  beating 
strongly  (Mackenzie) .  (Edema, 
ascites,  and  hydrothorax  may 
be  present  as  in  other  cardiac 
diseases. 

The  pulse  is  usually 
small  because  the  peripheral 
arteries  are  constricted  in  or- 
der to  maintain  the  blood- 
pressure,  which  may  be  per- 
fectly normal.  The  rhythm 
may  continue  regular  or  may  become  irregular  as  the  disease  advances. 
Still  more  common  are  attacks  of  heart  failure  and  drops5^ 
In  many  cases,  notably  those  of  Shattuck  and  Mackenzie,  such  attacks 
may  recur  at  intervals  during  a  decade  or  more.  At  first  the  condition 
yields  readily  to  rest  and  treatment,  but  later  the  attacks  become  more 
and  more  frequent  and  persistent. 


Fig.  234. — Diagram  showing  the  changes  in  the  circu- 
lation in  tricuspid  stenosis.  The  arrows  indicate  the  rise 
in  venous  pressure  in  the  right  auricle  (RA)  and  the  vena 
cava,  and  the  fall  in  pressure  in  the  pulmonary  artery 
(PA).  The  pressure  in  the  left  auricle  and  ventricle  niay 
remain  unchanged  or  may  fall. 


SYMPTOMS. 

Fortunately  for  the  patients,  the  course  of  tricuspid  stenosis  is  usually 
a  chronic  one,  the  development  of  the  lesion  generally  lagging  behind  the 
concomitant  stenosis  of  the  mitral  or  the  other  lesions  that  may  be  present. 
As  a  consequence,  the  lesion  may  be  present  for  a  number  of  years  without 
manifesting  any  signs  other  than  cyanosis,  and  no  symptoms  whatever. 
Osier  quotes  a  case  reported  by  Hirtz  and  Lemaire  who  was  known  as 
"Thomme  bleu"  for  two  years  before  he  developed  any  symptoms.  On 
the  other  hand,  in  the  case  mentioned  by  Shattuck  there  was  said  to  be  "  no 
cyanosis." 

There  is  nothing  pathognomonic  about  the  symptoms.  Dyspnoea  on 
the  slightest  exertion  sets  in  and  becomes  progressively  worse.  Pain 
down  either  arm  is  relatively  common,  occasionally  pain  about  the  right 
side  and  abdomen  due  to  distention  of  the  auricle  or  of  the  liver.  Sudden 
death  is  quite  common. 


TRICUSPID   STENOSIS. 


409 


PHYSICAL    SIGNS. 

On  inspection  the  extreme  cyanosis  is  striking,  and  there  may  be  dila- 
tation and  accentuated  pulsation  of  the  veins.  When  carefully  timed  this 
pulsation  is  seen  to  be  presystolic,  and  is  often  a  "double"  pulse  of  the 
physiological  type.  Those  characteristics  are  brought  out  more  clearly 
by  a  venous  tracing.    In  long-standing  cases  the  fingers  may  be  clubbed. 

The  lungs  usually  show  signs  of  bronchitis,  oedema,  or  often  of  tuber- 
culosis. Pulmonary  infarction,  with  the  presence  of  areas  of  consolidation 
and  the  expectoration  of  dark  red  or  "prune-juice"  sputum,  is  relatively 
common.  In  the  physical  exam- 
ination of  the  heart  the  real 
lesion  is  often  overlooked.  Ex- 
cept for  the  systolic  retraction 
over  the  right  ventricle,  there 
may  be  nothing  abnormal  on 
inspection.  The  area  of  cardiac 
dulness  is  increased  to  the  right, 
corresponding  to  the  dilated 
right  auricle;  occasionally  also 
to  the  left,  as  a  result  of  con- 
comitant lesions  other  than  the 
tricuspid  stenosis. 

Palpation  sometimes  re- 
veals a  presystolic  thrill  over 
the  lower  part  of  the  sternum 
and  just  to  the  left  of  the  latter, 
but  it  is  rarely  as  distinct  in 
the  former  situation  as  in  the 

latter  (due  to  concomitant  mitral  stenosis).  The  shock  accompanying  the 
first  sound  over  the  right  ventricle  may  be  tapping.  The  second  pul- 
monic shock  is  usually  less  marked  than  might  be  expected  to  result  from 
the  lesions  present. 

The  characteristic  sign  on  auscultation  is  the  pres- 
ence of  a  short  presystolic  rumble,  which  is  maximum  over  the 
base  of  the  sternum  and  different  in  character  from  the  presystolic  rumble 
heard  at  the  apex.  There  is  also  a  snapping  character  to  the  first  sound  in 
this  area,  and  it  may  be  accompanied  by  a  tricuspid  systolic  murmur. 
This  murmur  is,  however,  often  absent,  indistinct,  or  merges  so  gradually 
into  the  mitral  murmur  that  its  existence  is  not  noted.  Except  when  other 
lesions  are  present  the  second  aortic  and  pulmonic  sounds  are  not  as  loud 
as  might  be  expected. 

DIAGNOSIS. 

So  indistinct  are  the  murmurs  due  to  the  tricuspid  lesion  and  so  com- 
pletely are  they  overshadowed  by  those  of  the  mitral  or  other  orifices  that 
the  diagnosis  before  death  was  made  in  only  six  of  Leudet's  114  cases.  The 
correct  diagnosis  has  been  almost  equally  rare  since  then.  It  may  be  made 
with  certainty  in  the  presence  of  marked  cyanosis,  dilatation  of  the  right 


Fig.  235.  —  Cardiac  outline  and  distribution  of  the 
presystolic  rumble  and  t^napping  first  sound  in  tricuspid 
stenosis. 


410  DISEASES   OF  THE   HEART   AND   AORTA. 

auricle  (increase  of  dulness  to  the  right),  presystolic  thrill  and  rumble,  and 
presystolic  liver  pulsation.  But  these  signs  disappear  as  the  auricle  begins 
to  weaken,  and  in  very  many  cases  the  existence  of  the  lesion  is  one  that 
can  be  suspected  rather  than  proved. 

Case  op  Tricuspid  Stenosis. 

The  following  notes  are  from  one  of  the  rare  cases  in  which  the  diagnosis 
was  made  during  life.  This  diagnosis  was  made  by  Professor  T.  B.  Futcher, 
who  has  kindly  permitted  the  writer  to  make  use  of  the  notes. 

Mrs.  A.  J.,  aged  37,  entered  the  private  wards  of  the  Johns  Hopkins  Hospital  on 
April  30,  1909.  The  family  history  was  negative.  She  was  not  a  blue  baby; 
has  been  healthy  since  childhood,  but  subject  to  occasional  sore  throat.  She  has  never 
had  acute  articular  rheumatism.  At  the  age  of  nineteen  she  had  an  obscure  fever  lasting 
several  weeks. 

She  has  been  somewhat  short  of  breath  for  the  past  nineteen  years,  and  since  an 
attack  of  grippe  about  twelve  years  ago  has  complained  of  palpitation  on 
exertion  or  after  eating.  These  symptoms  became  much  more  marked  four  years  ago, 
when  oedema  of  the  feet  and  ankles  and  cyanosis  api^eared  for  the  first  time. 
This  condition  passed  off  under  treatment,  but  returned  again  two  years  later,  again  pass- 
ing off,  only  to  return  with  increased  severity  eight  weeks  before  admission.  During  this 
attack  she  has  been  blue  and  has  had    severe   orthopnoea. 

Note  by  Dr.  Futcher,  May  1,  1909:  "Patient  is  of  short  stature,  a  little  overstout; 
very  marked  cyanosis  of  ears,  lips,  cheeks,  and  finger-nails,  although  this  is 
nothing  as  compared  with  the  day  she  reached  Baltimore.  There  is  a  distinct  jaun- 
diced tint  to  the  face  and  sclerotics.  Propped  up  in  bed;  considerable  dyspncEa.  Tongue 
moist,  only  a  trifle  coated;  pupils  normal  size  and  equal,  react  to  light  and  accommodation. 

"  Still  impossible  to  count  pulse  at  wrist,  although  very  faint  beats  are  occa- 
sionally appreciable.  Thorax  well  formed,  expansion  good  and  equal  on  both  sides. 
Lower  left  axillary  region  expands  slightly  less  than  right.  Lungs  :  Right  side  clear 
throughout  front  and  axilla  on  percussion.  There  is  an  occasional  crackling  rale  heard  at 
the  base.  Fairly  numerous  fine  moist  rales  audible  throughout  whole  back.  Left  lung 
(in  semi-recumbent  posture)  flatness  reaches  to  level  of  fourth  interspace  in  anterior  axil- 
lary line.  In  midaxillary  line  it  reaches  nearly  to  apex  of  axilla,  and  in  posterior  scapular 
line  to  a  point  about  3  cm.  above  left  scapula.  Slight  movable  dulness  in 
front  with  change  of  position.  On  auscultation,  breath  sounds  are  harsh  above  and  below 
clavicle,  as  in  compensatory  breathing.  Below  level  of  flatness  there  is  absence  of  vocal 
fremitus  and  distant  tubular  breathing  and  distant  nasal  quality  of  the  voice  sound. 

''  Heart. — Point  of  maximal  impulse  seen  and  felt  in  fifth  interspace  11  cm.  to 
the  left  of  the  midstemal  line  and  just  in  the  mammillary  line.  There  is  very  slight  pre- 
cordial bulging,  but  practically  no  pulsation  or  heaving.  Systolic  shock  distinctly  tap- 
ping at  apex;  no  definite  thrill.  Relative  cardiac  dulness  commences  at  the  upper 
border  of  the  third  rib,  in  fourth  right  interspace,  extends  8.5  cm.  from 
midstemal  line,  and  merges  into  the  fluid  flatness  to  left,  but  apparently  dulness  extends 
considerably  outside  of  midline.  There  is  no  apparent  Rotch's  sign  to  the  right.  The 
absolute  cardiac  dulness  begins  at  the  upper  border  of  the  fourth  rib  at  the  left  sternal 
margin,  extends  to  right  sternal  margin  at  level  of  fourth  rib  and  to  point  of  maximal 
impulse  in  fifth  left  interspace.  On  auscultation,  the  first  sound  is  very  snap- 
ping at  apex.  There  is  as  yet  no  definite  presystolic  murmur,  but  there  is  a  slight  echo- 
ing rumble  in  diastole.  There  is  no  systoUc  bruit  at  the  apex.  The  second  sound  is 
not  audible  here.  In  the  fourth  and  fifth  interspace  at  the  left  ster- 
n a  1  border  the  snapping  quahty  of  the  first  sound  is  even  more  marked 
than  at  the  apex  and  the  tapping  systolic  shock  is  very  striking  here. 
The  second  sound  is  audible  and  there  is  definitely  reduplicated.  There  is  no 
rumbling  presystolic  murmur  here.  In  diastole,  however,  there  is,  on 
very  careful  auscultation,  a  faint,  soft,  prolonged,  blowing  diastolic 
murmur.  At  the  aortic  area  yesterday  there  was  a  faint  systolic  thrill. 
It  is  just  perceptible  this  morning.  The  first  sound  is  audible  and  is  accompanied 
by  a  very  rough  systolic   bruit  transmitted  upwards  to  stenoclavicu- 


TRICUSPID   STENOSIS.  411 

I  a  r  articulation.  The  second  aortic  is  quite  loud  and,  if  anything, 
accentuated.  There  is  no  aortic  diastolic  bruit  heard  here.  Pulmonic  sounds  clear, 
second  pulmonic  accentuated.    The  external  jugulars  are  only  slightly  distended. 

''Liver.  — Absolute  flatness  extends  from  sixth  rib  to  a  point  apparently  on  a 
level  with  the  costal  margin  in  right  mammillary  line.  In  median  line  it  reaches  only  to 
tip  of  ensifonn.  Owing  to  cedematcis  abdominal  walls,  it  is  not  possible  to  palpate  for 
liver  edge.     No  visible   or  palpable   liver   pulsation. 

"Abdomen  moderately  distended,  walls  oedematous,  tympanitic  in  elevated  and  flat 
in  dependent  portions.  Undoubtedly  some  ascites.  There  is  very  marked  oedema  of 
dependent  portions  of  trunk,  moderate  of  arms  and  hands,  very  marked  of  thighs  and  legs. 

" Over  dorsal  surfaces  of  both  wrists  there  are  quite  numerous  pin-head 
sized   petechia;." 

The  urine  was  very  scant  (300  c.c),  of  orange  color,  specific  gravity  1015,  acid,  con- 
tains a  trace  of  albumin  and  many  hyaline  and  finely  granular  casts. 

Her  chest  was  aspirated  by  Dr.  Henry  on  May  1,  and  500  c.c.  of  dark  straw- 
colored  clear  fluid  removed.  She  became  worse,  however,  and  her  kidneys  refused  to  act. 
On  May  3  her  pulse  became  irregular,  cyanosis  increased,  and  the 
petechial  eruption  on  the  dorsum  of  wrists  became  more  extensive.  She  died  at 
3.15  P.M. 

Intra  vitam  diagnosis  by  Dr.  Futcher:  Aortic  stenosis  and  insuffi- 
ciency,  mitral   stenosis,    probable   tricuspid  stenosis. 

Autopsy  showed  tricuspid,  mitral,  and  aortic  stenosis,  dila- 
tation and  hypertrophy  of  the  auricles,  contraction  and  atrophy  of  the 
ventricles,  chronic  passive  congestion  of  all  the  tissues  except  the 
lungs,  generalized  cedema,  pleural  and  pericardial  effusion,  compression  and  atelectasis 
and  oedema  of  the  lungs,  hemorrhagic  infarctions  of  lungs,  acute  diphtheritic  hemorrhagic 
colitis,  generalized  narrowing  of  arteries  and  thickening  of  veins. 

TREATMENT. 

Except  for  rest,  purgation,  and  palliative  treatment,  little  can  be  said 
in  this  condition.  Digitalis  is  sometimes  of  value  to  restore  tone  to  the 
auricle  and  increase  the  force  of  the  ventricular  contraction,  but  it  very 
frequently  fails.  In  the  spells  of  acute  heart  failure  a  free  venesection 
may  ward  off  impending  death  by  lowering  the  venous  pressure,  relieving 
the  heart  failure;  and  by  diminishing  the  viscosity  of  the  blood  may  afford 
more  lasting  relief.  Free  purgation  is  often  also  of  great  benefit,  because  it 
may  lower  the  pressure  in  the  veins. 

PROGNOSIS. 

The  prognosis  depends  entirely  upon  the  degree  of  stenosis  and  the 
rapidity  of  its  progress.  As  has  been  said,  this  is  frequently  very  chronic. 
Mackenzie's  famous  case,  which  is  typical,  was  a  woman  whose  lesion 
probably  dated  from  an  attack  of  rheumatism  in  1880,  at  the  age  of  twenty- 
nine.  In  1892  she  complained  of  weakness  and  shortness  of  breath,  and 
at  that  time  the  liver  showed  a  presystolic  pulsation.  She  was  subject  to 
numerous  temporary  attacks  of  extreme  heart  failure  and  died  in  1899. 
However,  this  woman  was  under  excellent  care  during  the  last  seven  years 
of  her  life,  and  lived  a  tolerably  discreet  and  hygienic  existence.  Had  she 
been  compelled  to  do  heavy  work  her  life  would  probably  have  been  much 
shorter. 


412  DISEASES   OF   THE    HEART    AND    AORTA. 

BIBLIOGRAPHY. 
Tkicuspid  Stenosis. 

Herrick,  W.  W.:  Tricuspid  Stenosis,  with  Report  of  a  Cure,'  Arch.  Int.  Med.,  Chicago, 
1908,  ii,  295. 

Huchard,  H.:  Maladies  au  coeur,  tome  iii,  Paris,  1905;  based  upon  statistics  of  Leudet, 
R.:  Essai  sur  le  retrecissement  tricuspidien,  Paris,  1888. 

Herrick.  J.  B.:  Tricuspid  Stenosis,  with  Report  of  Three  Cases  with  Autopsies,  etc.,  Bost. 
M.  and  S.  J.,  1897,  cxxxvi,  245. 

Goodhart,  Roy  and  Adami,  Weber  and  Deguy.     See  page  359. 

Gairdner.     Quoted  from  Herrick. 

Mackenzie,  J.:  Notes  on  a  Case  Presenting  some  Novel  Features  in  Cardiac  Symptoma- 
tology, Edinb.  Hosp.  Rep.,  1897,  v,  22.  Studies  on  the  Pulse  and  Movements  of  the 
Heart,  N.  Y.,  Edinb.,  and  Lond.,  1902. 

'  Probably  intended  to  be,  "with  Report  of  a  Case." 


IX. 

PREGNANCY  AND  LABOR  IN  CASES  OF  HEART  DISEASE. 

PULSE-RATE    AND    BLOOD-PRESSURE. 

The  effect  of  pregnancy  upon  the  heart  is  influenced  by  several  factors. 
The  gradual  pushing  of  the  diaphragm  as  the  uterus  grows  causes  the  heart 
to  assume  a  more  transverse  position  (raising  the  apex  to  the  fourth  inter- 
space in  28  out  of  35  cases  observed  by  Stengel  and  Stanton),  and  thus  plac- 
ing it  in  a  position  which  embarrasses  its  action.  Moreover,  a  reflex  vagus 
inhibition  is  often  present,  which  causes  the  pulse-rate  to  become  slowed. 
Blot  has  reported  a  pulse-rate  as  low  as  36;  40  per  cent,  of  Vegas's  cases 
were  slow,  but  only  26  per  cent,  of  Skabo's  cases  were  below  75  per  minute. 
There  is  also  an  increase  in  the  width  of  the  blood  channel  through  the 
uterine  vessels,  which  is  manifested  by  the  presence  of  a  dicrotic  pulse. 
Jn  order  to  overcome  these  factors  and  to  keep  up  the  equilibrium  of  the 
circulation,  the  heart  is  compelled  to  put  forth  increased  efforts.  Slemons 
and  Goldsborough  in  a  most  careful  series  of  observations  have  found  the 
following  figures,  which  accord  well  with  the  previous  findings  of  O.  Fellner, 
Stengel  and  Stanton,  and  Vogeler. 

They  found  the  following  figures  : ' 


Blood-pressures. 

PuL«<e- 
rate. 

Cardiac 

output 

P.P.  X  P.R. 

Work  of  heart. 

Max. 

Min. 

Pulse- 
pressure. 

Mean   pressure 
(min.+i  P.  P.) 

rate. 

Normal 

(Erlanger) 
Pregnancy . . . 

Puerperium . . 

110 
127 

115 

65 
74 

72.6 

45 

53 

49 
in  primig. 

60 
in  multip. 

42.5 

80 
91.6 

86.5 

72 
80.5 

70.5 

3240 

3325 

(primig.) 

5332 
(multip.) 

3000 

259,000 

Primig. 
195,000  to  429,000 

Multip. 
421,000to  1,065,000 

Primig. 
290,000  to  327,000 

Multip. 
156,000  to  337,000 

HYPERTROPHY. 


This  prolonged  increase  in  work  was  supposed  by  Larcher  to  bring 
about  hypertrophy  of  the  heart,  a  fact  which  has  found  some  support  in 
the  weighings  of  certain  observers;  but  the  more  careful  work  of  W.  Miiller 
and  of  later  observers  (average  weight  of  heart  during  pregnancy  227  Gm.) 


*  While  this  method  of  calculation  is  not  intended  to  be  regarded  as  quantitatively 
accurate  (see  p.  24),  it  shows  the  quaUtative  changes  fairly  well. 

413 


414  DISEASES   OF   THE   HEART   AND    AORTA. 

fails  to  substantiate  this  view.  The  increase  in  size  supposed  to  represent 
hypertrophy  is  probably  due  in  part  to  dilatation  of  the  heart,  and  in  part 
to  the  apparent  increase  in  cardiac  area  which  occurs  when  the  heart  lies 
in  a  more  transverse  position.  However,  a  very  slight  hypertrophy,  like 
that  of  the  athlete's  heart,  arising  from  the  slightly  increased  work  of 
the  heart  during  nine  months,  would  not  be  surprising.  During  labor  an 
additional  strain  is  thrown  on  the  heart,  but  this  is  of  comparatively  short 
duration. 

FUNCTIONAL    TRICUSPID    INSUFFICIENCY    AND    OVERSTRAIN    DURING    LABOR. 

James  Mackenzie  has  shown,  moreover,  that  the  dilatation  during 
pregnancy  affects  the  right  heart  particularly,  and  that  in  very  many  cases 
even  of  otherwise  normal  women  a  definite  insufficiency 
of  the  tricuspid  valve  may  appear,  disappear,  and  reappear  accord- 
ing to  the  condition  of  the  patient.  The  presence  of  this  insufficiency 
is  shown  by  both  the  positive  venous  pulse  and  the  systolic  murmur  in  the 
tricuspid  area.  The  effects  during  the  labor  pains  are  exactly  comparable 
to  those  of  heavy  lifting,  defecation,  etc.  (exercises  of  strain  of  maximal 
intensity),  and  are  accompanied  by  forced  expiration  with  glottis  closed 
(Valsalva's  experiment)  as  well  as  by  very  general  muscular  contractions. 
Dr.  Slemons  informs  the  writer  that  during  the  labor  pains  there  is  often  a 
rise  of  fifty  millimetres  of  mercury  in  the  maximal  pressure,  though  these 
elevations  are  of  short  duration.  It  is  therefore  not  surprising  that  some 
hearts  should  fail  and  that  pulmonary  csdema  should  be  an  occasional  com- 
plication, especially  in  mitral  stenosis  where  the  pulmonary  circulation  is 
already  engorged.  It  is  perhaps  surprising,  however,  that  so  few  cases  actu- 
ally succumb  during  the  strains  of  labor.  Schlayer's  results  typify  the  gen- 
eral experience  in  this  regard.  He  lost  eight  out  of  twenty-five  cases  (32  per 
cent.)  of  severe  heart  disease,  but  only  two  of  these  (8  per  cent.)  died  during 
labor.  From  this,  as  well  as  from  the  work  of  Slemons  and  Goldsborough 
and  the  metabolism  experiments  of  Williams  and  Slemons,  it  would  appear 
that  the  act  of  labor  itself  does  not  impose  a  much  more  severe  strain 
upon  the  organism  than  that  arising  during  the  course  of  pregnancy. 

CAUSE  AND  FREQUENCY  OF  DEATH  FROM  LABOR. 

The  immediate  cause  of  death  during  labor  is  usually  pulmonary 
oe de ma  from  failure  of  the  left  ventricle.  However,  as  above  stated,  only 
about  one-fourth  of  the  fatal  cases  die  during  labor,  the  greater  number 
surviving  some  days,  weeks,  or  months.  In  the  cases  of  mitral  stenosis, 
apoplexy  or  cerebral  embolism  is  not  uncommon,  owing  to  loosening  of 
thrombi  which  form  in  the  left  auricle  during  the  periods  of  stasis. 

As  regards  the  results  obtained  by  different  writers  in  cases  with  heart 
lesions  the  greatest  divergence  is  found.  The  following  represent  the 
mortality  reported  by  various  writers:  Macdonald  61  per  cent.,  v.  Guerard 
34  per  cent.,  Lublinsky  60  per  cent.,  v.  Leyden  55  per  cent.,  Schlayer  48 
per  cent.,  Wessner  49.3  per  cent.,  Lwoff  12  per  cent.,  Gusserow  6  per  cent., 
Jess  31.5  per  cent.,  Wiesenthal  12.5  per  cent.,  Schneider  7.1  per  cent., 
Miiller  3  per  cent. 


PREGNANCY  AND   LABOR   IN    HEART   DISEASE. 


415 


A  very  careful  study  of  these  conditions  has  been  made  by  O.  Fellner 
in  Schauta's  chnic  in  Vienna.  Fellner  noted  that  the  percentage  of  heart 
cases  reported  in  obstetrical  clinics  was  far  too  low  for  the  general  prev- 
alence of  cardiac  disease,  and  upon  careful  routine  examination  found  that 
about  six  cases  out  of  seven  of  compensated  heart  dis- 
eases were  actually  escaping  detection  in  the  clinics. 
So  little  effect  had  heart  disease  made  upon  the  course  of  pregnancy 
and  labor!  Of  the  cases  that  had  been  recognized  in  the  obstetrical 
clinic  in  ten  years  he  found  the  following: 


Cases. 


Mother 
died. 


ChUd 
died. 


Mitral  insufficiency, 

Compensated 26 

Uncompensated 14 

Mitral  stenosis,  ! 

Compensated i 

Uncompensated 4 

Mitral  stenosis  plus  insufficiency. 

Compensated 10 

Uncompensated 17 

Aortic  insufficiency, 

Uncompensated 

Aortic  insufficiency  plus  mitral  insufficiency, 

Compensated 

Uncompensated 


Total 


81 


2 
10 


26 


In  the  900  cases  occurring  since  his  own  routine  examinations  of  the 
heart  were  instituted,  he  found: 


Mitral  insufficiency, 

Compensated 

Uncompensated 

Mitral  stenosis  plus  insufficiency. 

Compensated 

Uncompensated .-rr:777^ TTT.  . . 

Aortic  insufficiency  plus  mitral  insufficiency, 
Compensated 


Cases. 

Mother 
died. 

Child 
died. 

14 

0 

4 

1 

0 

0 

3 

0 

1 

1 

1 

0 

1 

0 

0 

FACTORS    INFLUENCING    PROGNOSIS. 


These  statistics  from  unselected  cases  are  much  more  favorable  than 
the  previous  reports  would  indicate,  and  are  in  accordance  with  the  con- 
clusions of  Hicks  and  French  that  few  women  with  heart  disease  are  sterile, 
that  they  are  not  particularly  liable  to  abort,  and  that  most  of  them  bear 


416  DISEASES   OF   THE    HEART   AND    AORTA. 

children  well.  Blacker,  in  a  most  excellent  resume  of  the  subject,  coin- 
cides with  these  opinions,  but  finds  53  deaths  (12  per  cent.)  in  453  cases  of 
heart  disease  taken  from  the  literature. 

Most  writers  believe  that  the  variety  in  the  results  is  due  to  the  severity 
of  the  cases  which  happen  to  be  encountered,  or  at  least  recognized;  but 
the  excellent  statistics  from  Schauta's  clinic  would  indicate  that  skill  in 
the  management  of  the  case  plays  a  considerable  role.  It  must  not  be 
forgotten  that  the  recognition  of  an  organic  valvular  lesion  in  a  pregnant 
woman  may  be  by  no  means  easy,  for  the  functional  or  accidental  systolic 
murmurs  at  the  apex,  occurring  during  pregnancy,  may  closely  simulate 
those  from  an  organic  mitral  insufficiency;  and,  unless  their  disappearance 
is  noted  by  the  end  of  the  puerperium,  this  discrepancy  may  not  be  noted. 
The  constancy  of  the  murmur,  its  roughness,  its  transmission  to  the  axilla 
and  the  increase  rather  than  decrease  in  intensity  at  times  when  the  condi- 
tion of  the  heart  improves  favor  the  diagnosis  of  an  organic  n!\itral  insuffi- 
ciency; while  in  the  presence  of  a  soft  murmur  occurring  with  a  dilated  heart, 
a  rapid  pulse,  and  a  break  in  compensation  the  presumption  is  temporarily 
in  favor  of  the  more  common  functional  insufficiency.  The  diagnoses  of 
mitral  stenosis  and  of  aortic  insufficiency  are  probably  more  uniformly 
correct  and  present  less  difficulty. 

Broken  Compensation  in  Pregnancy. — On  the  other  hand,  it  may  be 
difficult  to  judge  when  compensation  should  be  considered  broken.  The 
pushing  up  of  the  diaphragm  by  the  pregnant  uterus  causes  some  short- 
ness of  breath;  anaemia  is  also  a  factor.  The  pressure  upon  the  pelvic 
veins  may  give  rise  to  oedema  of  the  feet  and  legs  and  even  of  the  genitalia. 
And,  moreover,  a  relative  tricuspid  insufficiency  of  muscular  origin  may  be 
present  as  a  result  of  the  pregnancy  without  organic  lesion,  but  may  never- 
theless give  rise  to  the  same  signs  and  practical  effects  as  the  latter. 

The  diagnosis  of  broken  compensation  in  pregnancy  therefore  depends 
upon  signs  which  are  relative  rather  than  absolute,  since,  as  Mackenzie 
shows,  a  certain  degree  of  broken  compensation  is  an  almost  normal  phe- 
nomenon in  the  later  months  of  pregnancy.  This  again  is  relative,  for 
some  women  are  almost  as  active  throughout  pregnancy  as  at  other  times, 
while  other  quite  normal  women  may  be  almost  invalids  throughout  the 
entire  period.  It  is  upon  degree  rather  than  upon  actual  symptoms  that 
the  diagnosis  of  a  pathologically  broken  compensation  should  be  made. 
Dyspnoea  and  cyanosis  on  very  slight  exertion,  such  as  quietly  walking  a 
distance  of  a  few  hundred  yards  or  less,  walking  up  a  few  stairs,  etc.,  and 
the  presence  of  a  small  rapid  pulse,  persistent  cough,  enlargement  of  the 
liver,  and  oedema  of  the  feet  and  legs  may  be  regarded  as  the  most  impor- 
tant symptoms.  The  earlier  in  pregnancy  they  occur  the  more  alarming 
they  are.  Persistent  dyspnoea  or  orthopnoea  and  cyanosis  alone,  especially 
in  the  presence  of  a  valvular  lesion,  are  in  themselves  most  significant 
and  should  warrant  immediate  attention, 

MANAGEMENT    OF    CASES    OF    HEART    LESIONS    IN    PREGNANCY. 

The  correct  management  of  a  case  of  heart  lesion  complicated  by 
pregnancy  is,  as  stated  by  Blacker,  to  treat  the  heart  disease 
without    regard   to   the    pregnancy   until   the    break   in 


PREGNANCY  AND    LABOR   IN   HEART   DISEASE.  417 

compensation  is  seen  to  persist,  and  then  to  termi- 
nate the  pregnancy.  In  other  words,  as  long  as  compensation  is 
good  the  patient  should  merely  be  carefully  watched  but  no  medication 
need  be  resorted  to.  At  the  first  signs  of  cardiac  weakening  and  dilatation 
(dyspnoea  and  cyanosis,  etc.,  on  slight  exertion)  absolute  rest  should  be 
insisted  on  and  digitalis  or  strophanthus  should  be  given.  This  procedure 
should  be  insisted  on  even  if  the  diagnosis  of  organic  valvular  lesion  is  not 
definite,  for  these  procedures  will  afford  quite  as  much  relief  in  cases  of 
functional  tricuspid  insufficiency.  Moreover,  they  should  be  repeated  at 
the  shghtest  indication  (see  page  180),  especially  toward  the  end  of  pregnancy. 
It  is  advisable  in  such  cases  to  give  a  few  prophylactic  doses  of  digitalis 
when  labor  seems  imminent,  or  a  few  doses  of  strophanthus  at  the  begin- 
ning of  labor  pains,  so  as  to  have  the  tonus  of  the  heart  muscle  at  its  opti- 
mum by  the  time  the  strain  of  the  second  stage  is  imposed  upon  it.  At 
periods  of  acute  dilatation,  and  especially  when  pulmonary  cedema  sets 
in,  venesection  affords  the  greatest  relief. 

If  cardiac  symptoms  disappear  the  patient  may  be  gradually  allowed 
up  and  around,  but  she  must  be  more  careful  than  before,  and  if 
signs  of  a  second  break  in  compensation  occur,  terminating  the  pregnancy 
should  be  seriously  considered.  This  is  especially  true  in  cases  of  mitral 
stenosis,  in  which  the  cardiac  accidents  of  pregnancy  are  particularly  fre- 
quent. Women  with  compensated  mitral  stenosis  may  pass  through  five, 
six,  or  seven  pregnancies  without  appearing  to  be  injured  by  them  (Len- 
hartz),  but  Avhen  cardiac  symptoms  appear  in  a  case  of  this  disease  during 
the  course  of  a  pregnancy  it  is  nearing  the  danger  line,  and  if  these  persist 
in  spite  of  rest  and  treatment  or  when  compensation  is  once  broken,  the 
danger  becomes  great. 

Fellner's  low  mortality  (21  cases  with  1  death)  is  probably  due  to  the 
careful  practice  of  Schauta's  clinic,  which  he  summarizes  in  the  advice  to 
''terminate  pregnancy  in  cases  of  mitral  stenosis  as  soon  as  the  slightest 
signs  of  broken  compensation  appear,"  or  in  cases  in  which  signs  of  danger 
had  been  present  in  previous  pregnancies. 

Case  of  Mitral  Stenosis  with  Pregnancy  and  Labor. 

The  danger  of  disregarding  this  advice  was  well  illustrated  by  a  patient  under  the 
writer's  care  during  the  past  year.  She  was  a  young  married  woman  of  twenty-six,  and 
was  seen  in  November,  1907,  in  the  sixth  month  of  pregnancy,  complaining  of 
shortness  of  breath  and  was  quite  cyanotic.  Her  trouble  dated  from 
the  birth  of  her  first  child  nine  months  before,  at  which  time  she  had 
evidently  received  a  mild  puerperal  infection..  The  veins  were  rather  full; 
her  heart  was  not  enlarged,  and  at  the  apex  the  first  sound  was  snapping 
and  preceded  by  a  "slight  presystolic  rumble.  This  varied  in  intensity  from  time 
to  time.  Occasionally  a  blowing  diastolic  murmur  was  heard  along  the  left 
border  of  cardiac  dulness,  but  not  over  the  aortic  area.  The  pulse  was  small 
and  weak,  not  collapsing,  usually  regular.  There  was  slight  oedema  of  the 
shins  and  ankles.  The  patient  was  placed  in  the  hospital,  and  her  condition  improved  at 
once,  so  that  \A-ithin  two  weeks  she  was  allowed  to  enter  the  waiting  ward  of  the  obstet- 
rical department.  It  was  then  proposed  that  labor  should  be  induced,  but  the  obstetrical 
house  staff  did  not  regard  the  case  as  imperative.  She  left  the  hospital  contrary  to  advice, 
and  on  January  1,  1908,  in  the  seventh  month  of  pregnancy,  she  was  deUvered  of  a 
healthy  premature  child.  The  labor  was  easy.  She  insisted  upon  giv- 
ing the  infant  the  breast  for  a  couple  of  weeks,  but  remained  in  bed  and  quiet,  suffering 
27 


418  DISEASES   OF   THE   HEART    AND    AORTA. 

from  orthopnoea.  This  continued  in  spite  of  digitalis.  Her  liver  was  enlarged,  and 
oedema  of  the  legs  gradually  set  in.  She  finally  returned  to  the  hospital,  but  never  recu- 
perated, and  died  in  June,  1908.  The  child,  which  had  always  been  under  the 
care  of  a  district  nurse  and  later  in  the  Thomas  Wilson  Hospital,  also  died  dur- 
ing the  same  month. 

Termination  of  Pregnancy. — In  an  almost  exactly  similar  case  Hellendal 
performed  an  abortion  as  soon  as  the  signs  of  broken  compensation  were 
definite,  and  eight  days  later  resected  both  tubes  to  prevent  subsequent 
pregnancy.  The  patient  made  a  perfect  recovery  and  her  life  is  no  longer 
endangered. 

In  deciding  the  question  of  terminating  pregnancy,  it  must  be  borne 
in  mind  that  in  from  25  to  40  per  cent,  of  patients  with 
severe  heart  lesions  the  pregnancy  does  not  reach 
term,  but  premature  labor  occurs  spontaneously  owing  to  partial  asphyxia 
of  the  fcetus.  The  placental  circulation  is  slowed,  the  aeration  is  poor,  and, 
as  Fellner  has  shown,  there  is  often  a  large  necrotic  border  about  the  pla- 
centa. This  probably  results  from  thrombosis.  Moreover,  the  statistics 
of  the  obstetrical  clinics,  even  of  Schauta's,  are  far  more  favorable  than  the 
end  results  would  show.  Our  own  case  above  mentioned  would  be  classed 
in  such  statistics  as  "improved"  at  the  end  of  the  puerperium  and  the 
child  as  "living";  while,  as  a  matter  of  fact,  both  died  within  six  months 
after  the  labor.  Since  most  statistics  are  compiled  from  the  histories  of 
hospitals,  where  the  cases  are  subsequently  lost  sight  of,  it  is  probable  that 
this  represents  a  very  large  class  of  cases.  The  children  are  especially  deli- 
cate, and,  even  if  they  survive,  succumb  more  easily  to  pulmonary  and  gastro- 
intestinal infections  during  the  first  or  second  year  than  do  other  children. 

The  inevitably  high  child  mortality  and  the  danger  to  the  mother, 
especially  in  mitral  stenosis,  somewhat  lessen  the  moral  responsibility  of 
terminating  pregnancy.  Moreover,  as  Weber  and  Deguy  have  shown, 
pregnancy  and  labor  are  in  themselves  causal  factors  in  valvular  disease, 
and  especially  mitral  stenosis,  through  the  occurrence  of  hemorrhages  into 
the  substance  of  the  valves  (see  Chapter  III),  or,  as  in  the  case  of  our 
patient,  bring  about  the  recurrence  of  a  slumbering  endocarditis,  and  thus 
leave  the  patient  worse  than  before,  often  with  a  progressive  lesion.  When 
it  has  been  decided  to  terminate  pregnancy,  this  should  be  done  as  soon  as 
possible.  The  procedure  of  choice  depends  upon  the  severity  of  the  symp- 
toms and  the  necessity  for  immediate  emptying  of  the  uterus.  They  have 
been  summed  up  by  Fellner  in  the  following  scale:  (1)  Induction  of 
labor  with  de  Ribes  bag  or  packing  the  cervix;  (2)  craniotomy;  (3)  forceps; 
(4)  version  and  extraction;  (5)  Cesarean  section.  In  general  it  must  be 
said  that  the  less  the  operative  interference  with  the  physiological  course 
of  each  stage,  the  less  shock  to  the  patient  and  the  better  the  end  result. 
On  the  other  hand,  each  stage  of  labor  is  likely  to  be  prolonged  in  such 
cases  and  this  must  be  avoided.  When,  the  condition  is  alarming,  the 
relief  should  be  rapid.  Pulmonary  oedema  is  often  at  once  relieved  by 
tapping  the  fetal  membranes,  removing  the  amniotic  fluid,  and  allowing 
the  diaphragm  to  descend;  although  the  labor  then  becomes  much  harder. 
The  patients  usually  stand  the  operative  interference  well.  As  in  other 
conditions,  ether  is  preferable  to  chloroform  where  the  heart  is  diseased. 


PREGNANCY   AND   LABOR   IN   HEART   DISEASE.         419 


AORTIC    DISEASE    IN    PREGNANCY. 

As  aortic  disease  is  comparatively  rare  in  women,  it  usually  receives 
little  mention.  It  is  significant,  however,  that  in  Fellner's  series  there  was 
a  very  high  mortaHty  (60  per  cent.)  in  the  foetus.  Newell  reports  a  case 
in  which  there  was  little  cardiac  discomfort  throughout  pregnancy,  but  a 
hard  labor  set  in.  Forceps  were  used.  Collapse  and  pulmonary  oedema 
ensued,  and  the  mother  died  four  hours  after  labor.  The  child  died  also. 
This  is  simply  an  example  of  the  acute  heart  failure  (probably  acute  dila- 
tation of  the  left  ventricle  with  sudden  onset  of  functional  mitral  insuffi- 
ciency) so  characteristic  of  aortic  insufficiency.  Mitral  lesions  are  usually 
more  dangerous  than  aortic,  but  they  usually  give  signs  of  gradual  progres- 
sion. The  danger  in  aortic  insufficiency  may,  as  in  Newell's  case,  come  on 
very  rapidly  and  result  in  the  death  of  the  patient. 

SUBSEQUENT    PRECAUTIONS. 

In  cases  in  which  dangerous  breaks  in  compensation  occur  during  the 
course  of  pregnancy  and  termination  of  the  latter  becomes  necessary,  as 
well  as  in  those  which  reach  a  natural  termination  under  conditions  in  which 
the  life  of  the  mother  is  endangered,  measures  must  be  taken  to  prevent 
subsequent  conception.  As  Feis  points  out,  the  physician's  advice  to  a 
married  woman  to  absolutely  avoid  coitus  is  so  rarely  followed  that  for 
practical  purposes  it  is  scarcely  worth  giving.  To  rely  entirely  upon  it 
therefore  savors  of  hypocrisy.  Feis  beheves  that  in  these  cases  prophylactic 
measures  against  conception  should  be  advised.  Fellner  and  Hellendal 
go  one  step  further.  They  both  advise  and  practise  sterilization  of  the 
mother  by  resection  of  the  tubes,  an  operation  which  is  not  fraught  with 
much  danger,  and  which  then  relieves  her  from  the  sword  of  Damocles 
that  otherwise  hangs  over  her  head. 

MATRIMONY    AND    HEART    DISEASE. 

The  question  also  arises  under  what  condition  may  women  with  heart 
disease  be  permitted  to  marry.  As  Fellner's  statistics  show,  the  danger 
is  not  very  great.  Blacker  sums  up  the  facts  in  the  statement  that  all 
women  with  heart  lesions  will  sufTer  from  them  sooner  or  later,  and  that 
this  period  need  not  be  much  accelerated  by  pregnancies.  Some  writers 
even  go  so  far  as  to  state  that  pregnancies  do  not  alter  the  duration  of  life 
at  all,  but  this  view  is  much  too  optimistic.  The  best  proof,  however, 
that  the  compensated  heart  lesion  should  not  be  a  bar  to  matrimony  is 
shown  by  Fellner's  statistical  proof  that  six  out  of  every  seven  heart  lesions 
are  not  even  suspected  in  the  average  obstetrical  clinic.  On  the  other  hand, 
if  compensation  is  poor,  marriage,  like  any  other  strain,  should  of  course 
be  forbidden.  This  again,  as  Fellner  points  out,  depends  as  much  on  socio- 
logical as  on  physical  factors,  for  a  woman  in  poor  circumstances  may  be 
able  to  live  more  quietly  and  avoid  cardiac  strain  more  readily  in  married 
life  than  when  supporting  herself  by  her  own  work.  Under  such  circum- 
stances the  patient  should  be  made  fully  aware  of  the  dangers  of  conception 
and  coitus.    All  things  being  considered,  compensated  mitral  stenosis  cannot 


420  DISEASES   OF   THE    HEART    AND    AORTA. 

be  made  an  exception  to  these  rules,  although  its  presence  warrants  a  cer- 
tain foreboding  in  the  physician  consulted,  and  should  direct  his  advice 
toward  the  side  of  caution.  If  compensation  has  once  been  broken  in  a 
case  of  mitral  stenosis,  conception  should  be  forbidden  and  marriage 
strongly  advised  against.  The  same  applies  to  well-marked  chronic 
myocarditis  or  nephritic  cardiopathy  when  these  can  be 
diagnosed  with  probability,  since  they  run  a  more  unfavorable  course  for 
both  mother  and  foetus  than  do  the  cases  of  valvular  lesions, 

BIBLIOGRAPHY. 

Stengel,  A.,  and  Stanton:  Heart  and  Circulation  in  Pregnancy  and  the  Puerperium,  Trans. 
Asso.  Am.  Phys.,  Phila.,  1904,  xix,  520. 

Vejas:  Mittheilungen  ueber  den  Puis  und  die  vitale  LungencapacitJit,  etc.,  Samml.  klin. 
Vortr.,  Leipz.,  1886,  No.  269. 

Szabo:  Ueber  die  Bradykardie  im  Wochenbette,  Frommel's  Jahresb.,  1901,  700. 

Slemons,  J.  M.,  and  Goldsborough,  F.  C:  The  Obstetrical  Significance  of  the  Blood- 
pressures  and  their  Relation  to  the  Work  of  the  Heart,  Johns  Hopkins  Hosp.  Bull., 
Bait.,  1908,  xix,  194. 

Fellner,  O. :  Herz  und  Schwangerschaft,  Monatschr.  f.  Geburtsh.  u.  Gynakol.,  Berl.,  1901, 
xiv,  370. 

Vogeler,  W.:  The  Blood-pressure  during  Pregnancy  and  the  Puerperium,  Am.  J.  Obstetr., 
1907,  Iv,  490. 

Macdonald,  A.:  The  Bearings  of  Chronic  Diseases  of  the  Heart  upon  Pregnancy,  Parturi- 
tion, and  Childbed,  Lond.,  1878. 

Leyden:  Ueber  die  Complication  der  Schwangerschaft  mit  chronischer  Herzkrankheit, 
Ztschr.  f.  klin.  Med.,  Berl.,  1893,  xxiii,  1. 

Schlayer,  Schneider,  and  Vinay.     Quoted  from  Feis. 

Miiller,  W.:  Die  Massenverhaltnisse  des  menschlichen  Herzens,  Berl.,  1878. 

Mackenzie,  J.:  Pulsations  in  the  Veins,  with  the  Description  of  a  Method  for  Graphically 
Recording  Them,  J.  Path.  u.  Bacteriol.,  Edinb.  and  Lond.,  1893,  i,  53. 

Schlayer.     Quoted  from  Fellner. 

Hicks  and  French.     Quoted  from  Blacker. 

Blacker,  G.  F.:  Heart  Diseases  in  Relation  to  Pregnancy  and  Labor,  Brit.  M.  J.,  Lond., 
1907,  i,  1225. 

Hellendal,  H. :  Herzfehler  in  der  Schwangerschaft  und  operative  Sterilisation,  Med.  Klinik, 
Berl.,  1907,  763. 

Newell,  F.  S.:  Valvular  Diseases  of  the  Heart  Complicating  Pregnancy,  Surg.,  Gynecol., 
and  Obstet.,  Chicago,  1907,  iv,  610. 

Weber  and  Deguy.     See  Part  III,  Chapter  III. 

Feis,  O.:  Ueber  die  Komplication  von  Schwangerschaft,  Geburt,  und  Wochenbett  mit 
chronischem  Herzfehler,  Samml.  klin.  Vortr.,  Leipz.,  Gynakol.    No.  78. 

The  articles  by  v.  Rosthorn  and  by  Lenhartz,  H.,  Die  Beziehungen  der  weiblichen  Gesch- 
lechtsorgane  zu  innere  Erkrankungen,  Verhandl.  d.  Kong.  f.  inn.  Med.,  Wiesb.,  1908, 
XXV,  29;  Tuszkai,  Uterus,  Graviditat  und  Herz,  ibid.,  1908,  xxv,  118,  and  the  sub- 
sequent discussion  contain  much  valuable  information. 


X. 

CONGENITAL  HEART  DISEASE. 

DEVELOPMENT  OF  THE  HEART. 

In  the  human  heart,  as  in  all  other  complex  anatomical  structures, 
there  are  many  portions  whose  form  and  function  are  obscure  and  difficult 
of  comprehension  when  considered  only  in  the  light  of  conditions  pres- 
ent in  the  adult,  but  which  become 
quite  clear  when  seen  in  the  various 
stages  of  their  development.  A 
brief  consideration  of  the  embryol- 
ogy of  the  heart  will  therefore  greatly 
simplify  the  study  of  the  anatomy. 
Moreover,  it  must  be  borne  in  mind 
that  occasionally  some  portion  of 
the  adult  heart  fails  to  develop 
beyond  the  embryonic  stage,  giving 
rise  to  the  signs  and  symptoms  of 
congenital  heart  disease;  and  there- 
fore a  knowledge  of  the  embryologi- 
cal  development  is  necessary  for  pur- 


FiG.  236. — Very  early  stage  in  the  development  of  the  human  circulatory  pyptem.  (Drawn  from 
a  model  of  a  iiuman  embryo  2.5  mm.  long,  about  two  weeks  after  fertilization.  From  Prof.  F.  P.  Mall's 
collection.  The  model  was  prepared  by  Mr.  W.  E.  Dandy.)  The  specimen  shows  the  two  aortse  (^40)  leading 
the  blood  to  the  chorionic  villi,  and  the  two  umbilical  veins  (UMB  V)  leading  it  back  to  the  primitive 
heart  (//).  The  five  branchial  or  aortic  arches  {A A)  which  connect  the  heart  with  the  aorta  are  sliown 
also.     A.  Dorsal  aspect.     B.   Lateral  aspect  of  the  head  end  of  the  same  embryo. 


poses  of  practical  diagnosis  and  prognosis  as  well  as  for  anatomical  study. 

The  earliest  stage  of  the  circulatory  system  in  the  mammalian  embryo 

consists  in  the  formation  of  a  number  of  small  blood-vessels  and  capillary 

421 


422 


DISEASES   OF   THE    HEART    AND    AORTA. 


plexuses,  which  arise  from  the  mesoblast  over  the  surface  of  the  yolk-sac. 
These  soon  unite  to  form  a  definite  symmetrical  vascular  system. 

Eternod  has  carefully  described  the  earliest  development  of  the  circu- 
latory system  in  a  human  embryo  1.2  mm.  long,  estimated  at  about  eleven 
days  after  fertilization.  Another  embryo  of  almost  the  same  age  (Fig.  236) 
has  recently  been  discovered  by  Dr.  Mall  and  modelled  by  Mr.  W.  E.  Dandy. 
In  this  embrj^o  the  venous  system  is  represented  almost  entirely  by  the 
umbilical  veins  {Umb  V),  which  carry  the  blood  that  has  been  aerated  in  the 
placenta  back  to  the  heart.  They  follow  the  border  between  the  embry- 
onic area  and  the  j^olk-sac  and  pass  forward  to  the 
head  end  of  the  embryo.  Here  (H)  the  two  veins 
unite,  and  at  the  union  there  are  given  off  a  second 
set  of  vessels  consisting  of  a  group  of  four  upon 
each  side,  the  aortic  arches  (A  A),  which  pass 
backward  more  or  less  parallel  to  the  midline 
and  soon  reunite  to  form  a  single  vessel  on  each 
side,  the  primitive  aorta}  (AO).  These  two 
aortse  carry  the  blood  from  the  embryo  proper 
back  on  each  side  of  the  midline  to  the  numer- 
ous ramifications  in  the  placenta,  whence,  as 
we  have  seen,  it  is  returned  through  the  umbil- 
ical veins.  At  this  stage  the  heart  is  simply  a 
small  dilatation  of  the  venous  tube,  and  the 
blood  is  propelled  by  the  pulsations  of  the  ves- 
sels throughout  their  entire  lengths.  There  is 
scarcely  a  widening  of  the  lumen  to  mark  the 
site  at  which  the  heart  will  develop, — namely, 
at  the  point  of  union  of  the  two  umbilical 
veins  just  behind  the  place  where  the  aortic  arches 
are  given  off. 

At  a  little  later  stage  (Fig.  237)  we  find 
the  heart  the  form  of  an  S-shaped  tube  just 
ventral  to  the  pharynx  of  the  embryo  to  which 
it  is  fixed,  and  already  two  dilatations  have 
taken  place  in  the  lumen,  forming  the  primitive 
sacs  of  the  ventricle  (F)  and  the  auricle  (atrium) 
(A).  The  point  of  union  of  the  veins  (sinus 
reuniens,  S  R)  has  been  pushed  further  backward.  The  umbilical  veins 
have  received  veins  entering  from  the  yolk-sac  (vitelline  veins)  as  well 
as  a  branch  (duct  of  Cuvier,  D  Cuv)  from  the  body  wall  on  each  side. 
The  duct  of  Cuvier  is  in  turn  formed  by  the  union  of  a  branch  to  the 
head  (jugular  vein,  Jug)  and  a  branch  (cardinal  vein,  Card)  extending 
downward  along  each  side  of  the  body  wall  and  giving  off  branches  to 
the  muscle  segments.  The  veins  to  the  intestine  arise  from  the  vitelline 
vein,  while  the  umbilical  or  omphalomesaraic  veins  continue  as  before 
to  carry  the  blood  back  to  the  placenta  and  yolk-sac. 

Anteriorly  the  arterial  portion  of  the  circulatory  system  may  now  be 
observed  to  be  composed  of  the  truncus  arteriosus  (Tr  A),  a  continuation 
of  the  ventricle,  and  four  aortic  arches  each  now  corresponding  to  a  definite 


Fig.  237. — Human  embryo  4 
mm.  long  (about  the  fourth  week 
after  fertilization),  showing  the 
further  development  of  the  heart 
and  of  the  branchial  or  aortic 
arches  (.4.4).  (Modified  from 
His.)  The  heart  has  assumed 
an  S  shape,  and  is  divided  into 
a  truncus  arteriosus  (TR  A),  a 
single  ventricle  (F),  and  a  single 
auricle  (AUR).  The  inner  en- 
dothelial cardiac  tube  (shaded 
light)  is  much  narrower  than  the 
outer  muscular  tube  (MUS). 
On  each  side  the  jugular  veins 
(JUG)  from  the  head  unite  with 
the  cardinal  veins  (CARD)  from 
the  trunk  to  form  the  duct  of 
Cuvier  (D  CUV)  which  empties 
into  the  sinus  reuniens  (S  R). 


CONGENITAL   HEART   DISEASE. 


423 


visceral  (or  gill)  arch  of  the  embryo  {V  A).     These  branches  of  the  aorta 
are  of  great  importance,  for  from  them  the  carotid,  axillary,  innominate, 
and  pulmonary  vessels  will  develop. 
As  the  embryo  grows  older  (Fig. 
240)  the  heart  is  still  more  S-shaped,  /    ^  ,■:( ao. 


Sept.V. 


Fig.  238. — Heart  of  an  embrj'o  slightly  older 
than  that  shown  in  Fig.  237,  allowing  the  earliest 
stages  in  the  formation  of  two  auricular  and  two 
ventricular  pouches.     (Drawn  from  a  His  model.) 


Fig.  239. — A  diagram  showing  the  interior  of 
this  heart;  AO.,  aorta  or  truncus  arteriosus;  SEPT. 
v.,  septum  of  the  ventricles;  OA  V.,  auriculoventric- 
ular  orifice;  CA.,  canalis  auricularis,  or  auricular- 
ventricular  channel;  AUR.,  auricles;  S.R.,  sinus 
reuniens,  or  common  chamber  into  which  the  two 
vense  cavae  empty,  which  corresponds  to  the  sinus 
venosus  of  the  lower  vertebrates. 


Fig.  240. — Schema  to  show  the  development  of  the  arterial  system  from  out  of  the  primitive  aortic 
arches.  A.  Schema  of  the  circulatory  system  at  about  the  same  stage  as  Fig.  237.  I-VI,  aortic  or  bran- 
chial arches  (the  fifth  branchial  arch  described  by  Tandler  arises  from  and  anastomoses  with  the  fourth, 
which  is  the  largest  of  the  branchial  arches).  AO,  AO,  primitive  aorta?;  PA,  PA,  rudimentary  pulmonary 
arteries;  V,  primitive  common  ventricle;  RA,  LA,  auricular  pouches.  B.  Schema  of  the  adult  arterial 
system  derived  from  the  aortic  arches.  EXT  CAR,  external  carotid  artery  (3d  arch);  INT  CAR,  in- 
ternal carotid  artery  (connecting  bars  of  first  three  arches);  COM  CAR,  common  carotid  artery  connect- 
ing bar  between  third  and  fourth  arches.  A.  The  aorta  is  seen  to  be  derived  from  the  fourth  branchial  arch, 
the  pulmonary  arteries  arise  along  the  course  of  the  sixth.  The  ductus  arteriosus  (Botalli)  represents  the 
distal  end  of  the  sixth  branchial  arch.  The  dotted  lines  indicate  the  outline  of  embryonic  arteries  which 
have  atrophied. 


and  at  the  junction  of  the  two  halves  of  the  S  a  small  crescentic  infolding 
of  the  muscular  and  endothelial  wall  has  begun  to  protrude  into  the  cavity 
of  the  ventricle  (interventricular  septum,  Sept.  V.),  while  the  ascending 
limb  of  the  lower  half  of  the  S  represents  a  stenosis  in  the  lumen,  the  canalis 
auricularis  (CA.),  whose  narrowest  part  forms  a  small  slit,  the  ostium 
auriculoventriculare  (atrioventriculare)   (OAV.). 


424 


DISEASES   OF  THE   HEART    AND    AORTA. 


The  development  of  the  interventricular  septum  continues  rapidly 
(Fig.  241),  and  also  a  similar  ridge  appears  running  longitudinally  along 
the  truncus  arteriosus,  changing  the  lumen  from  circular  to  U-shaped, 
each  arm  of  the  U  being  a  channel  leading  to  the  corresponding  half 
of  the  ventricle. 

The  auricular  (or  atrial)  cavity  is  now  also  widened  into  two  symmet- 
rical pouches,  the  right  and  left  auricles,  the  cavity  of  which  is  continuous 
with  the  junction  of  the  veins. 


Sept  V. 


Fig.  241. — A.  Heart  of  slightly  older  embryo  viewed  from  the  dorsal  aspect,  showing  the  separation 
of  the  aortic  and  the  pulmonary  channels  in  the  truncus  arteriosus.  (Drawn  from  a  His  model.)  B. 
Diagram  of  the  auricular  portion  of  the  .same  heart.  Lettering  as  in  Fig.  239.  VE,  Eustachian  valve, 
separating  the  sinus  from  the  auricular  portion  of  the  heart.  The  arrows  indicate  the  course  of  the 
blood-currents.  C.  Diagram  of  the  ventricular  portion  of  the  same  heart,  showing  the  course  of  the  cur- 
rents through  the  separate  channels  of  the  truncus  arteriosus. 


The  trunks  of  the  veins  have  already  undergone  considerable  changes, 
such  that  the  left  duct  of  Cuvier  is  now  atrophied,  and  most  of  the  blood 
from  the  head  and  upper  limb  returns  to  the  heart  through  the  right  duct 
of  Cuvier,  foreshadowing  the  superior  vena  cava,  while  the  blood  from  the 
placenta  returns  through  the  two  omphalomesaraic  (or  omphalomesen- 
teric) veins,  which  along  with  anastomoses  from  the  body  wall,  intestinal 
tract,  and  liver  will  form  the  inferior  vena  cava.  The  junction  of  the 
two  venae  cavse  forms  the  sinus  reuniens  which  opens  into  the  auricular 
cavity.  In  the  wall  of  the  sinus  reuniens  at  this  stage  there  is  a  longi- 
tudinal valve-like  fold  of  endothelium  {VE,  Fig.  241,  B),  so  arranged  that 
blood  from  the  superior  vena  cava  flows  over  it  into  the  right  auricle 
(atrium),  while  the  blood  arriving  from  the  placenta  is  directed  under  it 
into  the  left  auricle. 


CONGENITAL   HEART    DISEASE. 


425 


Fig.  242. — Still  later  stage,  showing  com- 
plete division  of  the  truncus  arteriosus  into 
pulmonary  artery  and  aorta.  (Drawn  from  a 
Born  model  of  a  rabbit's  embryo  10  mm. 
long.)  The  arrows  show  the  course  of  the 
blood-stream.     DA,  ductus  arteriosus. 


Very  shortly  after  this  stage  the  most  important  changes  take  place 

in  the  heart  (Fig.  242).     The  two  channels  of  the  truncus  arteriosus  are 

now  completely  separated  off  from  one 

another,   and  exist  as  distinct  vessels, 

the  aorta  (AO)  and  the  pulmonary  ar- 
tery (PA),  connected  with  each  other 

at   only  one   point  through  the  ductus 

arteriosus   (DA).      The  interventricular 

septum  (septum  ventriculorum,  Sept  V., 

Fig.  241,  C)  is  now  found  to  be  almost 

completely    closed,    and    the    originally 

single    auriculoventricular    opening    is 

now  divided  into  two  portions  (mitral 

and  tricuspid,  Mit.  and  Trie.)  separated 

by  the  ingrowth  of  the  septal  ridge.     In 

the    auricles    also    great    changes   have 

occurred.     The   greater  portion  of  the 

sinus  reuniens  has  been  drawn  into  the 

cavity  of  the  auricle,  and  exists  there  as 

a  separate  chamber,  whose  right  margin 

opening  into  the  right  auricle  is  formed  by 

the  longitudinal  valve  (VE)   (described 

in  connection  with  the  previous  stage  of 

development,  now  known  as  the  valvula  venosa  dextra,  or  Eustachian 

valve) .     The  left  wall  of  the  right  auricle  is  formed  by  the  septum  auricu- 

lorum,  which  has  grown  considerably, 
partly  through  the  gradual  ingrowth 
of  the  septal  ridge  and  partly  by  the 
pushing  in  of  a  mass  of  connective 
tissue  arising  from  the  latter  and  from 
the  left  wall  of  the  sinus  reuniens 
and  known  as  the  septum  inter- 
positum.  The  left  wall  formed  in 
part  by  the  wall  of  the  vein  is  imper- 
fect, and  on  the  left  the  cavity  extends 
over  to  the  auricular  septum  (sep- 
tum a  t  r  i  o  r u  m) .  This  septum  has 
also  not  completely  closed,  and  the 
reconstruction  (Fig.  243)  from  a 
model  by  Born  at  this  stage  shows  a 
double  opening  between  the  two  auri- 
cles. At  a  later  stage  (Fig.  245,  B) 
these  openings  have  broken  down 
into  one,  the  foramen  ovale,  and 
it  is  the  opinion  of  Born,  in  opposi- 
tion to  His,  Sr.,  that  the  latter  struc- 
ture   is    of  secondary   formation   and   does  not   arise   directly   from   the 

primitive  interauricular  openings,  although  it  performs  the  same  function, 

— namely,  of  allowing  the  blood  to  pass  from  the  right  into  the  left  auricle. 


Fig.  243. — Auricular  end  of  the  same  heart. 
The  blood  enters  through  the  superior  and  inferior 
vena  cava  (SUP.V.C,  INF.V.C.)  into  the  sinus 
reuniens  (SR),  wliich  is  separatetl  from  the  right 
auricle  {R.AUR.)  by  the  Eustachian  valve  {VE), 
which  at  this  stage  forms  a  large  partition  between 
thettwo  cavities.  The  foramen  ovale  (FOR.OV.) 
connects  the  sinus  reuniens  with  the  right  ventri- 
cle; it  is  divided  into  two  parts  by  a  thin  lamina 
formed  from  the  interauricular  septum.  TRIC, 
tricuspid  orifice;  P.V.,  pulmonary  veins. 


426 


DISEASES   OF   THE   HEART    AND    AORTA. 


In  the  later  stages  a  valve-like  flap  of  connective  tissue  projects  over  the 
foramen,  allowing  the  blood  to  flow  only  from  right  to  left. 


DEVELOPMENT    OF    THE    PERICARDIUM. 

The  pericardial  cavity  develops  as  a  part  of  the  original  body  cavity 
or  coelom,  from  which  it  is  separated  at  a  later  stage.  In  the  earliest  em- 
bryos (Fig.  236)  the  pericardial  cavity  arises  as  a  small  space  lined  with 
endothelium,  surrounding  the  blood-vessels  on  each  side  of  the  embryo 
(Fig.  244,  A).  These  two  spaces  or  cavities  unite  at  the  head  end  of 
the  embryo  to  form  a  single  pericardial  cavity  which  surrounds  the 
primitive  heart.     At  a  slightly  later  stage  the  heart  and  the  pericardial 


F    c 


Fig.  244. — Development  of  the  pericardial  cavity.  A.  Earliest  stage  in  the  development  of  the 
pericardial  cavity.  (After  Robinson.)  Embryo  corresponding  roughly  to  the  stage  shown  in  Fig.  236.  E, 
ectodenn;  C,  coelom;  En,  entoderm;  PB,  primitive  blood-vessel.  The  pericardial  cavity  is  repre.sented  by 
the  part  of  the  coelom  present  at  this  level.  B.  Later  stage  showing  the  division  of  ccrlom  into  pleural 
and  pericardial  cavity.  (Schematic.)  The  arrow  points  to  the  channel  connecting  the  two  cavities.  C. 
Relations  of  the  pericardium  in  the  adult.     (Schematic).     ANTER.  MEDIAST.,  anterior  mediastinum. 


cavity  lie  upon  the  ventral  aspect  of  the  pharynx  and  the  pericardial 
and  pleural  cavities  together  form  the  anterior  or  cephalic  portion  of 
the  coelom. 

At  a  later  stage  (Fig.  244,  B)  the  heart  has  grown  to  fill  almost  all  the 
ventral  portion  of  the  coelom  in  its  vicinity,  and  about  its  contour  the 
connective  tissue  of  the  body  wall  is  closing  in,  as  shown  by  the  arrow, 
beginning  to  divide  the  original  ccelomic  cavity  into  a  pleural  and  a 
pericardial  portion. 


CONGENITAL   HEART    DISEASE.  427 

In  Fig.  244,  C  this  closure  has  become  complete,  and  we  have, 
represented  in  rough  diagram,  the  conditions  present  in  the  adult  chest. 
The  pericardial  cavity  is  completely  separated  from  the  pleural  cavity, 
and  is  lined  throughout  by  a  single  layer  of  flat  endothelial  cells, — 
the  portion  growing  directly  upon  the  heart  called  the  epicardium, 
and  the  portion  forming  the  opposite  wall  of  the  pericardial  cavity,  the 
pericardium  proper. 

The  pleural  cavity  has  now  grown  more  extensive  than  before,  owing 
to  the  growth  of  the  lungs,  which  have  pushed  forward  along  the  sides  to 
well  in  front  of  the  heart  and  almost  to  the  midline,  leaving  a  narrow  pleural 
cavity  between  them  and  the  chest  wall.  Like  the  pericardial  cavity  the 
pleural  cavity  is  lined  with  endothelium  which  extends  parti)'  over  the 
lung  (visceral  pleura)  and  partly  along  the  thoracic  wall  (parietal  pleura). 
The  anterior  portion  of  the  visceral  pleura  passes  over  the  pericardium, 
from  which  it  is  separated  only  by  a  very  thin  mass  of  connective  tissue, 
occasionally  containing  fat-cells.  The  three  layers — pleural  endothelium, 
connective  tissue,  and  pericardial  endothelium — are  so  closely  fused  that 
together  they  are  generally  designated  as  the  pericardium,  of  which  one 
speaks  of  the  pleural  and  pericardial  surface.  The  pericardium  does  not 
extend  quite  to  the  chest  wall,  while  the  pleura  does  so,  and  ventral  to 
the  heart  we  find  a  small  space  filled  by  connective  tissue  and  known  as 
the    anterior   mediastinum. 


PHYSIOLOGY  OF  THE  FETAL  CIRCULATION. 

The  blood  of  the  foetus  is  aerated  in  the  placenta  and  passes  back 
through  the  umbilical  veins  and  through  the  ductus  venosus  (D.V.)  to 
the  inferior  vena  (V.C.I.),  without  passing  through  the  liver.  The  sinus 
reuniens  has  now  become  part  of  the  main  cavity  of  the  auricle,  and  the 
inferior  vena  cava  (V.C.I.)  empties  into  the  latter  near  the  septum  ventric- 
ulorum.  Over  its  mouth  pass  the  remains  of  the  Eustachian  valve  (val- 
vula  venosa  dextra)  which  directs  the  blood  not  into  the  right  auricle  but 
away  from  it  across  the  right  auricle  to  the  limbus  fossce  ovalis.  According 
to  the  views  of  Galen  and  Harvey,  the  blood  from  the  superior  vena  cava 
and  that  from  the  inferior  are  mixed  in  the  right  auricle  before  any  of 
the  stream  passes  to  the  left  auricle.  Haller  and  Sabatier,  however,  believed 
that  no  such  mixing  took  place,  but  that  all  the  blood  from  the  inferior  vena 
cava  (aerated  blood)  passed  across  to  the  left  auricle,  while  the  blood  from 
the  superior  vena  cava  passed  down  into  the  right  ventricle.  Pohlman 
has  recently  given  an  excellent  review  of  the  subject.  He  has  investigated 
it  experimentally  on  the  fetal  pig's  heart  by  injecting  starch  granules  into 
the  superior  vena  cava  in  some  living  fetal  pigs  and  into  the  inferior  vena 
cava  in  others.  The  hearts  were  then  removed,  and  the  bloods  in  the  two 
ventricles  and  auricles  were  shown  to  contain  the  starch  granules  in  equal 
amounts,  confirming  the  theory  of  Galen  and  Harvey.  Pohlman  introduced 
capillary  glass  tubes  into  the  two  ventricles  and  demonstrated  that  the 
pressures  within  them  were  equal.  The  blood  from  the  left  ventricle  passes 
at  first  to  the  innominate  and  carotid  and  subclavian  arteries,  below  which 
the  aorta  is  joined  by  the  ductus  arteriosus  Botalli.    The  blood  from  the 


428 


DISEASES   OF   THE   HEART    AND    AORTA. 


right  ventricle  passes  into  the  main  trunk  of  the  pulmonary  artery,  from 
which  about  one-fifth  enters  the  rami  passing  to  the  lungs  and  about  four- 
fifths  passes  onward  through  the  ductus  arteriosus  and  enters  the  descend- 
ing aorta.  As  the  ductus  arteriosus  carries  a  little  more  blood  than  the 
descending  aorta,  the  volume  of  blood  in  the  aorta  is  more  than  doubled 
and  the  lumen  considerably  widened  below  its  entry.  The  blood  below  this 
point  goes  to  the  kidneys,  the  alimentary  tract,  the  bladder,  and  the  lower 
limbs,  and  the  rest  goes  on  through  the  umbilical  arteries  {Umb.  A.),  to  be 
aerated  in  the  placenta  and  returned  as  described  above. 


FORAMEN  OVALE 
EUSTACHIAN  VALVE 


Fig.  245. — A.  The  circulation  in  the  fcetus  just  before  birth.  Course  of  the  blood  to  and  from 
the  placenta.  (Semi-schematic.)  UMB  A,  UMB  I',  umbilical  artery  and  umbilical  vein;  DV,  ductus 
venosus.  B.  The  heart  just  before  birth.  The  course  of  the  blood-stream  is  indicated  by  the  arrows. 
VCS,  VCI,  superior  and  inferior  vena  cava. 


These  are  the  conditions  present  up  to  the  time  of  birth.  After  the 
first  respiration  the  expansion  of  the  lungs  greatly  reduces  the  resistance 
in  the  pulmonary  circuit,  so  that  it  becomes  less  than  that  in  the  aorta, 
and  most  of  the  blood  is  diverted  from  the  ductus  arteriosus  into 
this  new  channel  of  low  resistance.  Hence  it  persists  only  a  year 
or  so  after  birth  and  soon  becomes  changed  into  a  simple  strand  of 
connective  tissue. 

On  the  other  hand,  the  pressure  in  the  left  auricle  becomes  greater 
than  that  in  the  right,  and  the  valve  of  the  foramen  ovale  is  therefore 
kept  closed  against  the  septum,  and  soon  becomes  organized  as  a  part 
of  the  latter. 

With  the  cessation  of  placental  circulation,  the  ductus  venosus  loses 
its  physiological  importance  and  soon  undergoes  atrophy  and  closure. 


CONGENITAL   HExVRT    DISEASE.  429 

CLASSIFICATION  OF  CONGENITAL  HEART  LESIONS. 

Classifications  of  congenital  heart  lesions  are  difficult,  and  from  a 
clinical  stand-point  not  always  satisfactory.  From  the  anatomical  stand- 
point they  may  be  classified  as  follows: 

I.  Malformations  about  the  heart. 

1.  Malformations  of  the  chest  wall  (ectopia  cordis). 

2.  Malformations  of  the  pericardium. 

II.  Abnormalities  in  the  position  of  the  heart. 

1.  Heart  on  the  right  side  (dextrocardia  or  dexiocardia) . 

2.  Position  of  all  the  organs  inverted  (situs  transversus). 

3.  Heart  situated  in  the  neck  (cervical  heart). 

4.  Heart  situated  within  the  peritoneal  cavity  (abdominal  heart). 

III.  Abnormalities  of  the  valvular  orifices. 

1.  Pulmonary  stenosis  or  atresia. 

2.  Supernumerary  or  defective  cusps  of  pulmonary  valves. 

3.  Tricuspid  stenosis  or  insufficiency;  malformation  of  the  valve. 

4.  Aortic  stenosis;  atresia  of  the  aorta;  malformations  of  the  aortic  valve. 

5.  Mitral  stenosis;  malformation  of  the  mitral  valve. 

IV.  Defects  in  the  septa. 

1.  Interventricular  septum. 

a.  In  the  septum  membranaceum. 

b.  In  the  muscular  part  of  septum  (below). 

2.  Interauricular  septum. 

a.  Defect  or  absence  of  valve  of  the  foramen  ovale. 

b.  Valve  normal  but  not  closed. 

c.  Defect  between  the  muscle  strands  in  the  lower  portion  of  interauricular 

septum. 
V.  Abnormalities  in  the  cavities. 

1.  Supernumerary  septa. 

2.  Cor  biatriatum  triloculare. 

3.  Cor  biloculare. 

4.  Cor  biventriculatum  triloculare. 

5.  Bifid  apex. 

6.  Double  heart. 

VI.  Deviations  of  the  septum  cordis  with  transposition  of  vessels. 
VII.  Persistence  of  ductus  Botalli. 
VIII.  Abnormalities  of  the  aorta. 

1.  Coarctation  of  the  aorta. 

a.  Above  the  ductus  arteriosus. 
6.  Below  the  ductus  arteriosus. 

2.  Hypoplasia  of  the  aorta. 

3.  Malformations  of  the  aortic  arch. 

IX.  Abnormalities  in  the  arrangement  and  formation  of  the  veins. 

GENERAL    CHARACTERISTICS. 

Such  a  purely  anatomical  classification,  though  sufficiently  complete, 
does  not  furnish  a  good  basis  for  the  study  of  the  cardiac  malforma- 
tions, because  it  does  not  take  into  account  the  relation  of  the  indi- 
vidual lesions  to  one  another.  For,  since  these  lesions  are 
usually  produced  in  groups  rather  than  singly,  it 
is  quite  as  important  from  a  clinical  stand-point  to  recognize  these 
groups  and  understand  their  effect  upon  the  circulation  as  to  recognize 
the  ind'vidual  lesions. 

Moreover,  as  will  be  seen,  the  mere  clinical  manifestations  show  great 
similarity  in  the  various  lesions,  and  may  be  summed  up  in  what  may  be 


430  DISEASES   OF   THE    HEART    AND    AORTA. 

termed  the  "syndrome  of  congenital  heart  lesions;"  or, 
in  the  words  of  Peacock  (1866),  ''the  characteristic  symptoms 
of  malformations  of  the  heart  —  cyanosis  (especially 
from  birth),  palpitation,  dyspnoea,  faintings,  occa- 
sional convulsive  attacks  and  lividity.''  Moreover,  the 
most  common  physical  sign  of  many  congenital  lesions  is  a  loud  superficial 
murmur,  most  intense  in  the  second  and  third  left  interspaces  at  the  sternal 
margin  in  both  systole  and  diastole  and  often  heard  over  the  entire  pre- 
cordium  and  the  arteries  as  well. 

ETIOLOGY. 

As  Lancereaux  has  well  said,  "cardiac  teratology  repre- 
sents the  pathology  of  intra- uterine  life."  The  chief 
pathological  conditions  which  affect  the  development  of  the  foetus  may 
be  classed  as — 

1.  Inflammation  (fetal  endocarditis  or  myocarditis,  the  formation  of 
adhesions  about  the  heart  or  vessels,  etc.). 

2.  Abnormal  torsions  of  the  cardiac  tube. 

3.  Underdevelopment  of  heart  or  branchial  arches. 

These  processes  lead  directly  to  the  production  of  malformations 
which  may  be  designated  as  primary  congenital  lesions,  such  as  stenosis 
and  atresia  of  the  pulmonary  artery,  transposition  of  the  great  vessels, 
stenosis  at  the  isthmus  of  the  aorta,  etc.  The  presence  of  these  lesions  in 
the  foetus  in  turn  exercises  its  effect  upon  the  circulation,  which  alters  the 
course  of  development  and  brings  about  secondary  congenital  lesions. 
The  developmental  mechanics  which  results  in  the  formation  of  such 
groups  of  lesions  is  well  illustrated  in  pulmonary  stenosis  and  atresia,  the 
commonest  of  congenital  heart  lesions  which  may  be  considered  as  the 
prototype. 

PULMONARY  STENOSIS   AND   ATRESIA.* 

The  commonest  of  all  the  primary  congenital  lesions  is  pulmonary 
stenosis,  occurring  in  254  (68  per  cent.)  of  the  366  cases  of  congenital  heart 
disease  reported  by  Peacock  and  by  Keith.  Two  causes  have  been  ad- 
vanced to  explain  its  occurrence:  (1)  endocarditis  in  fetal  life;  (2)  defec- 
tive development  of  the  pulmonary  artery. 

1.  Bouillaud  (1835)  ascribed  it  to  endocarditis  in  fetal  life. 
This  theory  seems  certainly  to  be  applicable  to  those  cases  in  which  the  semi- 
lunar valves  have  already  formed,  but  just  as  in  the  adult  have  fused  along 
the  lines  of  closure.  This  is  well  shown  in  Fig.  2^6  and  in  a  case  figured  by 
Peacock.  Moreover,  a  number  of  cases  have  been  reported  in  which  rheu- 
matism or  infectious  disease  in  the  pregnant  mother  has  led  to  the  occur- 
rence of  endocarditis  in  the  foetus.  On  the  other  hand,  it  must  be  borne  in 
mind  that  in  329  (82.5  per  cent.)  of  399  cases  of  pulmonary  stenosis  col- 
lected from  the  reports  of  Rauchfuss,  Vierordt,  and  Abbott  the  interven- 

'Atresia — (Greek  arp^ro^  (atretos),  not  perforated),  from  a  =  not,  and  T-pljaiq  =  a  bor- 
ing =  absence  or  extreme  constriction  of  any  natural  passage  or  opening  of  the  body. 


CONGENITAL   HEART    DISEASE. 


431 


tricular  septum  remained  incomplete,  indicating  that  the  primary  lesion 
had  taken  place  before  the  time  at  which  the  septum  had  closed  (eighth 
week  of  embryonic  life).  As  Osier  has  pointed  out,  "It  is  not  easy  to 
imagine  a  fetal  endocarditis  localized  to  so  small  an  area  as  the  pulmonary 
valves  must  be  before  the  eighth  week  of  fetal  life."    To  this  very  objec- 


FiG.  246. — Pulmonary  stenosis  due  to  fusion  of 
the  cusps.  (Drawn  from  a  specimen  in  the  Army 
Medical  Museum,  Washington,  D.  C.)  There  is 
also  a  patent  interventricular  septum. 


INF. 


Fig.  247. — Pulmonary  stenosis  due  to  a  lesion 
of  the  infundibulum.  (Drawn  from  a  specimen  in 
the  ,4rmy  Medical  Museum,  Washington,  D.  C.) 
INF,  infundibular  portion  of  the  right  ventricle. 


tion,  how^ever,  the  advocates  of  this  theory  might  reply  that  in  very  many 
cases  the  lesion  is  by  no  means  confined  to  the  cusps  of  the  valves,  but  in- 
volves the  entire  infundibulum,  over  which  the  endocardium  may  be  thick- 
ened and  shrivelled  (Fig.  247).  Nor  does  it  necessarily  follow  that  even 
though  the  interventricular  septum  has  once  closed  it  must  remain  so, 


PATENT 

INTERVENTRICULAR 

SEPTUM 


PULMONARY  ARTERY 
PULMONARY  ORIFICE 


Fig.  248. — Complete  pulmonary  atresia.  (Drawn  from  a  specimen  in  the  ,\rmy  Medical  Museum, 
Washington,  D.  C.)  The  pulmonary  artery  ends  as  a  blind  sac  (shown  by  broken  lines)  just  above  the 
dot  which  marks  the  closed  pulmonary  orifice. 

since  it  may  rupture  under  increased  pressure  or  ulceration  may  result 
from  the  fetal  endocarditis.  Such  phenomena  have  occasionally  been 
observed   (Abbott) . 

2.  The  malformation  may  also  arise  by  ''irregular  evolution 
of  the  branchial  arches."  Panum  has  shown  that  malformations 
can  be  produced  experimentally  in  birds  by  raising  the  temperature  of 
incubation  (fever  in  the  mother) ;  and  His  believes  that  at  least  a  consider- 


432 


DISEASES   OF   THE   HEART    AND    AORTA. 


able  portion  of  malformations  result  from  "disturbances  of  developmental 
conditions  caused  by  insufficient  nourishment,  insufficient  aeration  of  the' 
blood,  and  mechanical  causes  resulting  from  malpositions  of  the  uterus,  dis- 
turbed placental  circulation,  etc." 

It  must  be  recalled  that,  as  shown  by  Rathke  in  1843,  the  pulmonary 
artery  separates  from  the  rest  of  the  truncus  arteriosus  about  the  eighth  week 
of  embryonic  life,  along  with  the  remains  of  the  sixth^  left  branchial  arch 
which  forms  the  ductus  arteriosus  and  the  right  pulmonar}'  artery  which 
springs  directly  from  this  arch  (Figs.  240  and  249) .  The  right  pulmonary 
artery,  according  to  Bremer,  has  sprung  in  a  similar  manner  from  the  right 
fifth  branchial  arch,  but  the  latter  has  atrophied  and  is  now  represented 

only  by  the  small  segment  con- 
necting the  right  pulmonary 
artery  with  the  truncus  pul- 
monalis.  In  the  twisting  of  the 
cardiac  tube  and  separation  of 
the  ventricles  the  part  of  the 
truncus  arteriosus  corresponding 
to  the  pulmonary  artery  pro- 
trudes ventrally  while  the  aortic 
portion  protrudes  dorsally.  The 
truncus  pulmonalis  thus  repre- 
sents the  ventral  half  of  the 
truncus  or  bulbus  arteriosus  and 
springs  directly  from  the  in- 
f  undibulum  of  the  right  ventricle 
(Fig.  249).  Stenosis  or  atresia 
.  may  therefore  take  place  from 
arrest  of  development  in  three 
places:  1.  In  the  trunk  of  the 
pulmonary  artery  between  the 
semilunar  valve  and  the  point 
of  branching, — i.e.,  where  the 
pulmonary  artery  is  in  close 
contact  with  (and  perhaps 
pressed  upon  by)  the  main  trunk  of  the  aorta.  (This  condition  is  represented 
in  a  case  of  Peacock's  series.)  2.  At  the  orifice  itself  (as  in  Fig.  246), 
from  fusion  or  stenosis  of  the  valves.  3.  Below  the  valves  and  within  the 
infundibulum  of  the  right  ventricle,  as  in  Fig.  247.  In  some  cases  a 
supernumerary  septum  may  separate  the  infundibulum  from  the  main 
cavity  of  the  right  ventricle,  thus  producing  the  so-called  third  ventricle. 
Peacock  regarded  this  structure  as  representing  the  condition  present 
in   the   turtle,    but   states   that    "such    separation"    (into    two   cavities) 


Fig.  249. — Schema  illustrating  the  genesis  of  pul- 
monary stenosis.  A.  Fusion  of  the  cusps.  B.  Fetal 
endocarditis  affecting  the  infundibulum.  C.  Normal 
mode  of  development  of  the  aortic  branchial  arches. 
D.  Maldevelopment  of  the  sixth  branchial  arch,  leading 
to  pulmonary  atresia. 


'  Rathke,  His,  and  the  older  writers  sfjeak  of  the  last  branchial  arch  from  which  the 
pulmonary  artery  arises  as  the  fifth  branchial  arch;  but  Tandler  (Zur  Entwickkmgsges- 
chichte  der  Kopfarterien  bei  den  Mammalia,  Morphol.  Jahrb.,  I>eipz.,  1902,  xxx,  275)  has 
recently  shown  that  a  small  rudimentary  arch  is  present  upon  the  same  stem  with  the 
fourth.  He  terms  this  small  arch  (which  plays  no  important  role  in  development)  the 
fifth,  and  the  pulmonary  arch  accordingly  becomes  the  sixth. 


CONGENITAL   HEART    DISEASE.  433 

"may  be  produced  in  different  ways.  It  may  depend  simply  on  undue 
development  of  the  ordinary  muscular  bands,  or  on  this  in  conjunction 
with  thickening  of  the  endocardium  or  subjacent  fibrous  tissue."  Re- 
cently Arthur  Keith,  of  London,  has  revived  Peacock's  idea  that  this  is 
the  portion  of  the  heart  which  is  homologous  with  the  bulbus  cordis  of 
the  lower  animals,  and  which,  as  Greil  has  shown,  becomes  incorporated 
into  the  substance  of  the  ventricle  (infundibulum)  just  as  the  sinus  is 
swallowed  up  by  the  auricle.  Keith  believes  that  the  period  during 
which  this  is  taking  place  represents  the  crucial  epoch  in  the  production 
of  malformations.' 

Certain  it  is  that  most  fetal  lesions  arise  about  the  time  when  the 
pulmonary  artery  and  the  aorta  and  the  remnants  of  the  branchial  arches 
are  taking  their  final  form,  the  interventricular  septum  is  becoming  com- 
plete, and  the  original  portions  of  the  branchial  arches  are  disappearing, — 
i.e.,  between  the  fourth  and  the  eighth  week  of  fetal  life. 


SECONDARY    MALFORMATIONS. 

As  has  been  stated  above,  stenosis  of  the  pulmonary  orifice  results 
in  stasis  within  the  right  ventricle,  and  the  blood  is  forced  to  take  a 
new  channel. 

Patent  Interventricular  Septum  with  Pulmonary  Stenosis. — In  80  per 
cent,  of  the  cases  of  pulmonary  stenosis  the  interven- 
tricular septum  is  still  open,  and  the  blood  is  forced  through 
the  open  septum  and  passes  up  through  the  aorta.  As  the  condition  is  a 
permanent  one,  the  current  through  the  septum  continues  and  its  closure  is 
prevented  (stasis  theory  of  William  Hunter  and  Kussmaul) .  In  rare  cases, 
and  especially  those  in  which  the  stasis  appears  at  a  very  early  stage,  the 
blood  current  eddies  through  and  keeps  open  a  passage  between  the  muscle 
strands  at  the  base,  in  contrast  to  the  usual  defect  at  the  septum  mem- 
branaceum.  This  opening  at  the  base  of  the  septum  is  often  accompanied 
by  defects  in  the  mitral  or  tricuspid  valves. 

Dextroversion  (Rechtslage)  of  the  Aorta.  —  Moreover,  the  pressure 
upon  the  septum  tends  to  deflect  it  toward  the  left  and  still  further  enlarge 
the  septal  opening  (Figs.  248  and  250) . 

In  most  cases  the  deflection  of  the  septum  to  the  left  is  so  great  that 
the  aorta  comes  to  lie  in  the  axis  of  the  right  ventricle.  The  cavities  thus 
come  to  form  an  inverted  Y  whose  arms  are  formed  by  the  ventricles  and 
whose  shaft  is  the  aorta.  Since  the  shaft  is  inclined  to  the  right,  this  gives 
the  appearance  as  though  the  aorta  arose  directly  from  the  right  ventricle 
(Rechtslage — dextroversion  of  the  aorta).  This  condition  is  present  in 
the  majority  of  the  cases  reported  by  Abbott,  especially  in  those  in  which 
there  is  complete  atresia  of  the  pulmonary  artery  (Fig.  248) . 

» It  is  possible  that  in  some  cases,  like  those  figured  by  Keith,  the  rudimentary  septa 
represent  endocardial  pockets  upon  the  wall  of  the  ventricle.  Schminke  (Endokardiale 
Taschenbildung  bei  Aorteninsuffizienz,  Arch.  f.  path.  Anat.,  etc.,  Berl.,  1908,  cxcii,  50) 
has  shown  that  similar  pockets  may  be  formed  in  the  left  ventricle  by  the  impact  of  a  re- 
gurgitant blood  stream. 
28 


434 


DISEASES   OF   THE    HEART   AND    AORTA. 


Open  Ductus  Botalli. — When  the  stenosis  reaches  a  considerable  grade, 
much  of  the  blood  that  reaches  the  lungs  must  pass  to  them  from  the  aorta 
back  through  the  ductus  arteriosus  (Botalli)  (Fig.  256),  which  is  therefore 

forced  to  remain  open  after  birth. 

Open  Foramen  Ovale.  —  If  the 
intraventricular  septum  has  closed 
before  the  pulmonary  stenosis  has 
occurred,  the  resulting  stasis  causes 
a  rise  of  pressure  in  the  right  auricle, 
and  the  path  of  least  resistance  to 
blood  flow  is  through  the  foramen 
ovale  to  the  left  auricle.  The  stream 
in  this  direction  is  therefore  larger 
than  usual  and  prevents  the  initial 
sclerosis  about  the  foramen,  or  even 
preserves  a  channel  in  the  lower  part 
of  the  septum,  so  that  sometimes  (as  in 
Fig.  250)  the  valve  of  the  foramen  may 
close  and  a  breach  through  this  por- 
tion of  the  septum  still  remain  patent. 
Three=chambered  Heart  (Cor  bia= 
triatum  triloculare) .  —  When  the 
atresia  is  complete  and  the  intraven- 
tricular septum  is  closed,  the  right 
ventricle  becomes   converted  into   a 

.^^^^^^^^K  ^^     blind  sac  into  which  no  more  blood 

W  ^^^^BBl^'^^^sa^^^     ^^^  enter.     The  tricuspid  orifice  thus 

^^j;..     -^^^I^B^^^B^S^^w         ^^^  iiito  disuse,  and  the  valve  under- 

^  '       ""  Ufflr^^^^^^HBB^^  gogg  stenosis  and   atresia  until  it  is 

completely  closed.  The  cavity  of  the 
right  ventricle  remains  only  as  a  small 
blind  sac  in  the  wall  of  the  left,  from 
which  the  aorta  arises,  cor  biatriatum 
triloculare  (Fig.  251). 

Lesions  of  the  Peripheral  Vessels. 
— The  abnormalities  in  structure  sec- 
ondary' to  congenital  heart  diseases  are 
by  no  means  confined  to  the  heart,  but 
especially  involve  the  finer  ramifica- 
tions of  the  vessels.  Recent  experimen- 
tal investigations  throw  much  light 
upon  the  distribution  and  formation 
of  these  abnormalities  in  a  manner 
which  is  of  great  practical  importance. 

J.  Loeb  in  1893  was  the  first  to  demonstrate  experimentally  the  effect  of  injury  to 
the  heart  upon  development.  He  poisoned  the  hearts  of  fish  (Fundulus)  embryos  by  tem- 
porary immersion  in  1.5  per  cent.  KCl  solution,  and  found  that,  though  the  hearts  of  such 
embryos  did  not  beat  at  all,  nevertheless  these  embryos  reached  adult  stage,  and  differed 
from  normal  fish  chiefly  in  the  irregular  structure  of  their  blood-vessels.  Knower,  working 
with  frog  tadpoles,  has  recently  confirmed  Loeb's  observations,  but  studied  the  changes 


Fig.  250. — Currents  and  lines  of  force  in  the 
embryonic  heart  which  result  from  pulmonary 
stenosis  and  tend  to  produce  patency  of  the  septa 
and  of  the  ductus  arteriosus.  A.  Ventricular 
end  of  the  fetal  heart  (before  the  eighth  week  of 
embryonic  life).  B.  Auricular  end  of  the  fetal 
heart  at  the  same  stage.  P  A,  pulmonary  artery; 
D  A,  ductus  arteriosus  (Botalli);  R  A,  right  auri- 
cle; R  V,  right  ventricle;  L  A,  left  auricle;  L  V, 
left  ventricle;  F  O,  foramen  ovale.  The  large 
arrows  indicate  blood  currents,  the  black  within 
the  ventricles,  the  white  those  within  the  auricles. 
The  small  arrows  indicate  the  forces  tending  to 
dilate  the  heart  and  to  deflect  the  septa.  In 
cases  of  extreme  grades  of  pulmonary  atresia 
the  current  in  the  ductus  arteriosus  flows  from 
aorta  to  pulmonary  artery,  instead  of  in  the 
reverse  direction. 


CONGENITAL   HEART   DISEASE. 


435 


in  more  detail,  and  has  found  that  after  mechanical  or  chemical  (acetone-chloroform) 
injury  to  the  heart  the  embryos  usually  become  very  oedematous  and  are  less  advanced 
than  the  controls.  These  embryos,  according  to  Mall,  are  very  similar  to  the  oedematous 
moles  frequently  met  with  in  gynaecological  practice.  Knower  also  found  that  the  devel- 
opment of  the  brain,  intestines,  liver,  and  pancreas  is  retarded,  "both  arteries  and  veins 
are  very  much  distended,  and  follow  very  irregular  courses.  ...  Inmost  cases 
the  first  precapillary  loops  are  represented  by  large  sinuses, 
.  .  .  .  but  there  is  a  notable  absence  of  capillaries  in  the  fin.  The 
smaller  vessels  do  not  push  out  nor  form  characteristic  plexuses.  Their  development  is 
inhibited.  The  weaker  the  heart-beat  in  fact  the  less  does  the  blood  flow  outward  from 
the  larger  vessels  and  precapillary  loops."  Similar  changes  had  already  been  described 
by  Panum  and  Dareste  in  chick  embryos,  by  Stockard  upon  fish  embryos  poisoned  with 
lithium,  and  by  Bardeen  upon  toads  which  had  been  fertilized  with  sperm  previously 
exposed  to  the  action  of  X-rays.  Knower  also  notes  that  similar  malformations  are  com- 
mon in  frogs  at  the  end  of  the  breeding  season  (when  the  sperm  may  well  be  weakened). 

The  secondary  changes  in  man,  outside 
of  the  heart,  are  quite  homologous  with  those 
in  animals.  These  are  especially  underdevel- 
opment in  stature  and  in  intelligence  and  the 
occurrence  of  malformations  of  the  arterioles 
and  venules.  Just  as  in  Knower's  frogs,  there 
is  a  dilatation  and  irregularity  of  venules  often 
in  the  skin,  viscera,  and  retina  (Fig.  253), from 
which  hemorrhages  frequently  take  place. 
Thickening  and  clubbing  of  the  ends  of  the 
fingers  (clubbed  fingers,  Fig.  254)  also  take 
place,  from  proliferation  of  the  connective 
tissue  as  a  result  of  the  venous  stasis. 


RUD, 


PATHOLOGICAL    PHYSIOLOGY. 


Fig.  251. — Three-chambered  heart 
(cor  biatriatum  triloculare)  produced 
by  complete  atresia  of  the  pulmonary 
and  tricuspid  orifices.  (From  a  speci- 
men in  the  Army  Metlical  Museum, 
Washington,  D.  C.)  RCD,  rudimen- 
tary cavity  corresponding  to  the  right 
ventricle;  F  O,  foramen  ovale.  The 
arrows  indicate  tlie  course  of  the 
blood  stream. 


The  effect  of  pulmonary  stenosis  upon  the 
mechanics  of  the  circulation  in  the  adult  is 
very  marked.  In  the  first  place  it  brings 
about  a  fall  in  blood-pressure  (both  arterial 
and   venous)  in  the   pulmonary   artery   and 

in    the    lungs   (Fig.   252),    and    consequently   a   corresponding   secondary 
lowering   of   pressure    in    the    aorta. 

The  extent  to  which  other  areas  of  the  circulatory  system  are  affected 
depends  as  much  upon  the  correlated  defects  as  upon  the  stenosis  itself. 
If  the  stenosis  is  the  only  lesion,  it  produces  a  fall  of  pressure  in  the 
pulmonary  artery,  a  rise  of  pressure  (from  stasis)  in  the  pulmonary  veins, 
and  a  marked  increase  in  pressure  within  the  right  ventricle,  like  that 
which  Liideritz  found  in  the  left  in  aortic  stenosis  (Fig.  252,  light  broken 
line).  This  always  leads  to  hypertrophy  of  the  right  ventricle  and  right 
auricle,  and  usually  to  the  signs  of  congenital  venous  congestion  to  be 
described  later. 

Between  these  two  grades  of  severity  there  exist  all  stages  of  cardiac 
insufficiency,  the  most  important  being  the  overloading  or  weakening  of 
the  right  ventricle,  which  leads  to  transitory  venous  stasis,  tricuspid  insuf- 
ficiency, and  cyanosis.    The  pressure  in  the  pulmonary  vein  and  left  auricle 


436 


DISEASES   OF   THE    HEART    AND    AORTA. 


is  by  virtue  of  tlie  pulmonary  stenosis  lower  than  usual,  while  that  in  the 
right  auricle  is  for  the  same  reason  higher.  Accordingly  the  tendency  is 
for  venous  blood  to  pass  into  the  left  auricle  and  ventricle  in  diastole  to  a 
much  greater  degree  than  when  the  pulmonary  orifice  is  normal,  and  hence 
to  cause  a  greater  tendency  to  cyanosis  and  dyspnoea  than  in  the  uncompli- 
cated patent  foramen  ovale. 

When  the  foramen  ovale  is  patent  but  the  septum  ventriculorum  closed 
(12  per  cent,  of  Abbott's  cases),  the  effect  upon  the  circulation  varies. 
Owing  to  the  pulmonary  stenosis,  the  path  of  least  resistance  is  through 
the  open  foramen  ovale  into  the  left  auricle  without  passing  through  the 
lungs,  and  much  blood  may  circulate  in  this  way.  Whether  or  not  this 
gives  rise  to  cyanosis  depends  upon  the  actual  amount  entering  the  lungs 
through  the  pulmonary  artery.     Under  ordinary  circumstances  this  may 


NORMAL 


PULMONARY 

STENOSIS 


PULMONARY 

STENOSIS 
AND  ATRESIA 


'  Fig.  252. — Diagram  of  the  circulation  in  pulmonary  stenosis  and  atresia.  Simple  pulmonary  stenosis. 
The  arrows  show  the  fall  of  pressure  in  the  aorta  and  pulmonary  artery  and  the  rise  of  pressure  in  the  vena 
cava  and  right  auricle.  The  broken  line  indicates  the  high  intraventricular  pressure  in  the  rignt  ventricle. 
Pulmonary  atresia,  with  patent  interventricular  septum  (SV).  patent  ductus  arteriosus  {DA ),  and  patent 
foramen  ovale  (FO).  The  blood  current  passing  through  the  patent  interventricular  septum  is  indicated 
by  the  heavy  broken  line;  the  light  broken  lines  indicate  intraventricular  pressure.  The  shaded  curves 
indicate  mixed  blood.  BR.  bronchial  arteries.  The  relation  of  the  new  channels  to  the  other  arteries 
is  shown  in  the  diagram  below. 


keep  enough  blood  aerated  to  avoid  cyanosis,  but  in  exercise  or  exertion 
when  more  COj  is  produced,  this  excess  may  show  in  the  patient's  color. 
Moreover,  the  venous  pressure  may  rise  until  the  pressure  in  the  right 
auricle  still  further  exceeds  that  in  the  left,  and  thus  a  larger  proportion 
of  this  non-aerated  blood  enters  the  left  side  of  the  heart,  giving  rise  to  the 
vicious  circle  of  the  open  foramen  ovale  (Fig.  250,  B). 


Cyanosis, 
Asphyxia 


/•     Increased  work  of  heart    \ 


\  Passage  of  unaerated  blood     ^^^ 
into  left  auricle 


High  pressure  in 
vena  cava 


SYMPTOMS. 


The  classical  picture  of  pulmonary  stenosis  and  especially  of  pulmonary 
atresia  is  the  "morbus  coeruleus"  or  "blue  sickness,"  as  which  it  has  been 
known  since  the  time  of  Senac  (1749).    The  patient  is  usually  a  small  child 


CONGENITAL   HEART   DISEASE.  437 

or  youth  below  the  normal  size  and  intelligence.  He  is  said  to  have  been 
blue  at  bi  r t  h  (as  in  74  of  Peacock's  101  cases),  or  to  have  become  so 
during  the  first  year  or  two  of  life  (as  in  almost  all  of  Peacock's  other  cases). 
He  has  suffered  from  cough  most  of  his  life,  as  well  as  shortness  of  breath. 
The  latter  becomes  extreme  or  may  come  on  in  severe  paroxysms  after 
exertion.  During  these  attacks  of  dyspnoea,  the  patient  may 
become  extremely  blue  or  even  black  in  the  face,  and  they  may  end  in  a 
fainting  spell  or  an  epileptiform  convulsion  (due  to  venous  stasis 
and  cerebral  ischsemia) .  He  may  also  have  frequent  headaches.  His 
hands  and  feet  are  usually  cold  (venous  stasis).  He  is  subject  to  frequent 
bleedings  from  the  nose,  mouth,  intestines,  or  other  mucous  membranes 
(due  to  congestion  in  dilated  venules),  which  may  even  suggest  the  diagnosis 
of  haemophilia. 

On  the  other  hand,  persons  with  a  considerable  grade  of  congenital 
pulmonary  stenosis  may  remain  free  from  symptoms  and  even  perform 
heavy  work,  as  in  the  case  quoted  by  Peacock  of  a  man  of  forty-four  who 
worked  as  a  navigator  until  six  weeks  before  his  death.  Such  cases,  however, 
constitute  only  a  small  percentage  of  every  series. 

Pulmonary  Stenosis  with  Patent  Interventricular  Septum. — However, 
when  the  interventricular  septum  is  defective  the  condition  is  entirely 
different.  The  lowered  pressure  in  the  pulmonary  artery  usually  continues 
unless  fully  compensated  by  the  anastomotic  circulation.  The  right  ven- 
tricle hypertrophies  until  it  equals  or  even  exceeds  the  left  in  thickness, 
and,  owing  to  the  dextroversion  of  the  aorta,  sends  its  large  quota  of  blood 
into  the  aorta.  The  pressure  in  the  systemic  veins,  therefore,  depends  not 
upon  the  pressure  within  the  right  ventricle  but  upon  the  ability  of  the 
right  ventricle  to  force  the  blood  onward  and  prevent  it  from  accumulating 
in  the  veins.  The  presence,  extent,  or  absence  of  symptoms,  on  the  other 
hand,  depends  upon  the  aeration  of  blood  in  the  lungs.  Peacock  well  says 
that  "  in  cases  of  this  description  the  open  state  of  the  foramen  ovale  and 
the  imperfection  in  the  ventricular  septum,  so  far  from  adding  to  the  danger, 
really  afford  the  means  of  relief  to  the  overcharged  right  auricle  and  ven- 
tricle without  which  life  could  not  be  prolonged  for  any  considerable  period." 
That  the  outlook  in  cases  where  defective  septa  accompany  the  pulmonary 
stenosis  is  graver  than  in  cases  where  the  stenosis  occurs  alone  is  due  merely 
to  the  fact  that  in  the  latter  case  the  lesion  is  usually  formed  late  in  fetal 
life,  and  hence  is  comparatively  mild;  or,  if  formed  early,  it  is  too  slight  to 
give  rise  to  the  stasis  which  keeps  the  septa  open, 

PHYSICAL    SIGNS. 

The  patients,  usually  children,  are  of  stunted  growth,  with  eyes 
watery,  veins  of  forehead,  face,  and  arms  large,  very  numerous,  and 
anastomosing  frequently. 

Cyanosis.— So  striking  and  so  frequent  is  the  occurrence  of  intense  cya- 
nosis in  congenital  heart  disease  that  this  term  has  become  almost  synony- 
mous with  the  "morbus  coeruleus"  (blue  sickness)  described  by  Senac. 

The  patients  may  be  persistently  livid  or  the  cyanosis  may  be  present 
only  at  times  of  exertion  or  ill  health.    It  may  then  come  in  attacks  asso- 


438  DISEASES   OF   THE   HEART    AND    AORTA. 

ciated  with  dyspnoea  and  sometimes  convulsions.     The  patients  may  be- 
come quite  black  in  the  face  and  may  remain  so  for  some  time. 

The  mode  of  origin  of  the  cyanosis  in  congenital  heart  disease  is  a 
noatter  not  only  of  scientific  interest  but  of  the  greatest  jjractical  importance  in  diagnosis 
and  prognosis.  Theories:  1.  Mixture  of  venous  with  arterial  blood.  Senac  (1749),  William 
Hunter,  Forget,  Meckel,  Corvisart,  Gintrac,  P^avre,  Paget,  and  others  supposed  that  the 
cyanosis  was  due  to  the  passage  of  venous  blood  directly  into  the  left  auricle  or  ventricle 
through  the  open  foramen  ovale  or  interventricular  septum.  While  this  may  play  a  role 
in  some  or  indeed  in  most  cases,  Moreton  Stille  (1844)  has  shown   "that    complete 

admixture   of    the    blood    may    take    place    without    cyanosis 

This  is  conclusively  demonstrated  by  the  two  following  cases. 

"First. — Foramen  ovale  open;  pulmonary  artery  arose  from  both  ventricles,  gave 
off  pulmonary  branches,  and  formed  the  aorta  descendens.  The  aorta  gave  off  the  branches 
to  the  head  and  upper  extremities  and  joined  the  pulmonary  artery  by  the  ductus  arterio- 
sus.    No   cyanosis.     Age  eight  months. 

"Second. — Heart  with  two  ca^ities;  aorta  and  pulmonary  arising  from  the  ventricle. 
No  cyanosis.     Age  eleven  days." 

Numerous  other  observations  in  the  literature  have  confirmed  Stille's  contention. 
On  the  other  hand,  when  there  is  mixing  of  venous  and  arterial  blood,  a  relatively  slight 
stasis  or  cardiac  weakness  from  overstrain  or  disease  may  bring  about  intense  cyanosis, 
which  would  not  occur  in  [>ersons  with  healthy  hearts. 

2.  The  second  theory,  proposed  by  Morgagni  (1761)  and  subsequently  advocated  by 
Louis.  Bouillaud,  Valleix,  Hasse,  Stille,  and  Rokitansky,  was  that  owing  to  the  pulmonary 
stenosis  there  was  sta.sis  in  the  systemic  veins,  and  that  the  cyanosis  resulted  from  that 
factor  only.  To  this  theory  Grancher  adds  the  fact  that  the  capillaries  and  precapillaries 
are  already  markedly  dilated  (for  reasons  given  above  on  page  434)  and  that  in  these  dilated 
capillaries  slight  stasis  brings  about  marked  cyanosis. 

Another  factor,  to  which  attention  has  been  called  by  Vaquez,  Osier,  and  others,  is 
that  in  such  cases  cyanosis  is  usually  accompanied  by  intense  polycythaemia,  and  the  in- 
crease in  the  amount  of  the  COj  haemoglobin  intensifies  the  cyanosis  which  might  other- 
wise be  present  in  moderate  degree. 

None  of  these  theories,  however,  explains  the  absence  of  cyanosis  in  cases  where  all 
the  venous  blood  passes  into  the  aorta.  In  these  cases  the  ventricles  are  strongly  exerting 
both  their  suction-pump  and  force-pump  action,  so  that  blood  does  not  accumulate  in 
the  veins.  On  the  other  hand,  the  pressure  in  the  aorta  (ranging  from  90  to  120  mm.  Hg) 
is  about  three  times  as  high  as  the  pressure  normally  present  in  the  pulmonary  artery, 
and  hence  is  capable  of  forcing  a  very  large  amount  of  blood  through  the  wide  bronchial 
arteries  or  open  ductus  arteriosus  (Botalli)  to  the  lungs. 

Whether  admixture  of  venous  blood  will  or  will  not  produce  cyanosis  depends  largely 
upon  the  amount  of  CO2  which  the  abnormal  pulmonary  circulation  can  take  care  of,  and 
which  in  most  cases  is  more  limited  than  in  the  normal  individual.  When  excessive  exer- 
cise, strain,  or  cardiac  weakening  causes  an  abnormal  increase  of  COj,  cyanosis  makes  its 
appearance,  and  owing  to  the  congenital  dilatation  of  the  capillaries  the  cyanotic  effect 
is  magnified. 

The  cases  in  which  cyanosis  occurs  in  spells  are  probably  examples  of  transitory 
venous  stasis  (in  congenitally  enlarged  capillaries  and  capillary  plexus).  In  cases  with 
open  foramen  ovale  stasis  in  the  systemic  veins  and  right  heart  will  divert  an  abnormally 
large  amount  of  venous  blood  through  the  foramen  ovale  (Fig.  250). 

The  head  occasionally  shows  signs  of  other  abnormalities  in  form.  There  may  be 
deficient  formation  of  bones  of  skull,  abnormalities  in  the  form  of  the  ears,  hare-lip,  cleft 
palate,  etc. 

Vascular  Changes  in  the  Retina. — Marked  changes  in  the  vessels  of 
the  retina,  seen  upon  examination  with  the  ophthalmoscope,  were  first 
reported  by  Knapp  in  1861.  In  cases  with  marked  cyanosis  elsewhere 
there  are  often  irregularities  in  the  lumina  of  arteries  and  veins,  which  are 
tortuous  ("resembling  large  angle-worms,"  Posey)  and  in  some  places 
very  wide  (twice  as  wide  as  normal),  in  others  very  narrow.    "Both  veins 


CONGENITAL   HEART   DISEASE. 


439 


I  ^ 


Fig.  253. — Dilatatiori  ami  1 1  regularity  of  the  reti- 
nal vessels.   V,  vein;  J.,  artery.    (After  Posey.) 


and  arteries  become  much  darker  than  normal,  the  former  assuming  a  deep 
violet  color,  while  the  arteries  resemble  normal  veins.  The  peripheral 
twigs  of  the  retinal  vessels  are  distended,  and  vessels  which  are  usually 
invisible  may  be  seen  over  the  entire  fundus Small  hemor- 
rhages are  of  frequent  occurrence  "  (Posey)  (Fig.  253) .  In  doubtful  cases 
this  feature  may  be  of  great  diag- 
nostic value,  but  it  can  be  expected 
to  occur  only  in  those  cases  in  which 
there  is  a  considerable  degree  of  cy- 
anosis and  in  which  the  prenatal 
slowing  of  circulation  has  probably 
been  marked. 

Clubbed  Fingers  (Hippocratic  Fin= 
gers). — The  ends  of  the  fingers  under- 
go peculiar  changes  (clubbed  fingers, 
Hippocratic  fingers)  (Fig.  254),  which 
also  occur  in  chronic  pulmonary  dis- 
eases, tuberculosis,  chronic  cardiac 
disease,  especially  in  children  and  in 
conditions  producing  long-continued 
local  or  general  venous  stasis  (Eb- 
stein).     The  change  is  confined  to  the 

pulp  of  the  finger,  which  is  thicker  than  normal  and  broadest  near  the  tip, 
and  tapers  in  a  proximal  instead  of  a  distal  direction.  The  nails  are  very 
convex  in  both  longitudinal  and  transverse  diameters.  They  are  usually 
cyanotic.  The  form  of  the  bones  is  practically  unchanged.  E.  Ebstein 
has  collected  a  large  number  of  observations 
which  prove  that  clubbing  of  the  fingers  and  toes 
results  from  chronic  passive  congestion  either  gen- 
eral or  local  (from  pressure  on  veins).  The  earlier 
in  intra-uterine  or  in  extra-uterine  life  that  the 
congestion  occurs  and  the  longer  is  its  duration 
the  more  marked  is  the  clubbing. 

The  occurrence  of  clubbed  fingers  is  dependent 
on  almost  the  same  factors  as  cyanosis,  and  the  two 
features  usually  occur  together  or  are  both  absent. 
Cardiac  Signs. — The  precordium  almost  always 
bulges,  and  the  wavy  systolic  impulse  over  the 
precordium  due  to  systole  of  the  right  ventricle  is 
usually  seen.  A  systolic  impulse  at  the  apex  may 
or  may  not  be  present.  The  area  of  cardiac  dulness 
is  usually  enlarged  to  both  right  and  left.  On 
palpation  a  rough  systolic  thrill  is  felt  over  the  pulmonary  area, 
from  which  it  is  transmitted  diagonally  upward  toward  the  left  clavicle 
and  downward  over  the  precordium  (Fig.  255).  In  cases  in  which  there 
is  a  defect  in  the  septum  ventriculorum,  this  thrill  is  also  intensified  over 
the  third  and  fourth  left  interspaces  near  the  sternal  margin. 

The  characteristic  sign  of  pulmonary  stenosis  on  auscultation  is  a  sys- 
tolic   murmur   accompanying  the  above-mentioned  thrill  and  following 


Fig.  254. — Clubbed  fingers. 


440 


DISEASES   OF   THE   HEART    AND    AORTA. 


Fig.  255. 


-Distribution  of  the  pulmonary  systolic  mur- 
mur of  pulmonary  stenosis. 


the  first  sound,  loudest  over  the  pulmonary  area  or  just  beyond  it  in  the  sec- 
ond left  interspace.    In  sharp  contrast  to  the  murmur  of  aortic  stenosis,  it  is 

transmitted  upward  and  to 
the  left.  It  is  also  heard 
over  the  precordium,  but,  un- 
less the  interventricular  septum 
or  ductus  arteriosus  (Botalli)  is 
open,  it  is  not  usually  trans- 
mitted to  the  systemic  arteries. 
The  second  pulmonic  sound  is 
either  absent  or  suppressed  in 
spite  of  the  respiratory  distress. 
However,  it  is  noteworthy  that 
in  those  cases  in  which  there  is 
uniform  pulmonary  atresia  ex- 
tending over  one  or  two  cm. 
and  where  the  lesion  is  actually 
most  severe,  the  murmur  may 
be  entirely  lacking.  The  same 
applies,  of  course,  to  complete 
obliteration  of  the  pulmonary  artery.  Needless  to  say,  the  imperfectly 
formed  valves  may  be  insufficient  and  a  diastolic  murmur  due  to  regurgi- 
tation may  also  be  present.  However,  a  murmur 
of  this  type  is  most  frequently  due  to  the  defect 
in  the  interventricular  septum  (see  page  444). 
Open  foramen  ovale,  when  present,  rarely 
gives  characteristic  signs,  but  occasionally  may  be 
diagnosed  from  a  presystolic  murmur  heard  at  the 
base.  The  signs  due  to  an  open  ductus  arteri- 
osus Botalli  are  so  similar  to  those  of  pulmo- 
nary stenosis  that  even  in  typical  cases  it  is 
almost  impossible  to  diagnose  in  the  presence 
of  the  latter.  The  murmur  from  the  former 
is  more  frequently  heard  at  the  back  to  the 
left  of  the  third  and  fourth  dorsal  vertebrae 
with  every  marked  inspiratory  accentuation 
and  expiratory  diminution  (Fran9ois-P>anck). 
The  chest  is  usually  poorly  expanded,  often 
pigeon-breasted.'  Harrison's  grooves  are  often 
prominent.  Signs  of  phthisis  (areas  of  dul- 
ness,  tubular  breathing,  increased  vocal  fremitus 
and  rales)  are  very  common,  especially  at  the 
apices  (SO  per  cent,  of  Abbott's  cases),  in  cases 
which  have  passed  the  age  of  infancy,  and  tuber- 
cle bacilli  are  frequently  found  in  the  sputum. 


Fig.  256. — Direction  of  blood- 
streams and  propagation  of  mur- 
murs accompanying  defect  in  the 
inter\-entricular  septum,  pulmon- 
ary stenosis,  and  open  ductus  arte- 
riosus (Botalli).  DEF.  SEPT., 
defect  in  the  interventricular  sep- 
tum; P.  ST.,  pulmonary  stenosis; 
PAT  DA,  patent  ductus  arterio- 
sus (Botalli);  1,  2,  3.  4,  5  represent 
the  corresponding  ribs. 


'  This  flatness  of  the  chest  may  perhaps  be  of  reflex  origin,  since  F.  Kauders  (Ueber 
einige  Experimente  zur  Lehre  von  der  cardialen  Dyspnoe,  Wien  klin.  Wchnschr..  1891), 
under  v.  Basch's  direction,  has  shown  that  the  diaphragm  rises  when  the  blood  flow  through 
the  lungs  is  diminished. 


CONGENITAL   HEART   DISEASE. 


441 


Condition  of  Other  Organs.  —  The  abdomen  is  often  very  full,  the 
liver  and  spleen  enlarged,  especially  in  cases  with  cyanosis  and 
venous  stasis.     The  genitalia  are  usually  underdeveloped. 

The  blood  count  usually  ranges  between  6,000,000  and  9,000,000,  the 
hsemoglobin  between  110  and  130  per  cent. 

There  are  often  albumin  and  casts  in  the  urine,  which  is  frequently 
scanty.    Occasionally  there  is  blood  from  the  dilated  capillaries. 


DIAGNOSIS. 

As  stated  by  Rauchfuss  in  1878,  the  diagnosis  of  congenital  pulmonary 
stenosis  can  usually  be  made  from  the  following  symptom  complex :  "  Cyan- 
osis, from  birth  or  following  signs  of  cardiac  affection  which  were  then  pres- 
ent; signs  of  dilatation  and  hypertrophy  of  the  right  auricle  and  ventricle; 
systolic  murmur  and  thrill  over  the  conus  arteriosus  and  pulmonary  artery, 
not  transmitted  to  the  carotid  arteries."  He  admits,  however,  as  do  all 
subsequent  authors,  that  the  exact  diagnosis  of  the  secondary  lesions  intra 
vitam  is  almost  impossible,  owing  to  the  multiplicity  of  the  lesions  which 
may  occur  and  the  fact  that  so  many  of  the  signs  overlap  one  another. 


TREATMENT  AND  PROGNOSIS. 

As  regards  prognosis  statistics  vary  considerably.  Of  Stoelker's  53 
cases  32  died  at  birth,  12  during  the  first  year,  and  11  during  the  first  decade. 
Only  4  reached  the  fourth  decade. 

The  age  of  death  in  Abbott's  series  was  as  follows: 


Pulmonary  Stenosis. 

Pulmonary  Atresia 

Age  at  death. 

V.  S.  closed. 

F.  0.  closed, 
delect  V.S. 

F.  0.  patent, 
defect  V.  S. 

1 

V  t!   „i„=«fi      F.  0.  closed, 
\  .  S.  closed.     ^,^fg^^  y  g 

F.O.  patent, 
defect  V.S. 

Before  1  year 

1-7' 

7-14 

14-20 

20-28 

28-45 

0 
2 

4 
3 
6 

1 

4 
16 
5 
8 
3 
0 

3* 

8 

4 

5 

0 

0 

6 
0 

2 

0 
0 

6 

2 
3 
0 
0 
0 
0 

lot 

0 
0 
0 
0 
0 

61 

36 

20 

5 

10 

*  9.7  per  cent. 


t  78  per  cent. 


One  can  hardly  fail  to  be  struck  by  the  contrast  between  the  cases  of 
pulmonary  atresia  and  pulmonary  stenosis,  since  78  per  cent,  of  the  former 
die  in  the  first  year,  while  this  is  the  case  in  only  9.7  per  cent,  of  the  latter. 
Even  of  these  only  36  per  cent,  survived  the  age  of  puberty  and  only  one 
reached  middle  age. 

In  the  individual  case  the  physician  may  be  guided  by  the  intensity 
of  the  sj^mptoms  even  more  than  by  the  physical  signs,  severe  symptoms, 
as  a  rule,  portending  an  early  death.     When  the  symptoms  in  early  youth 


442  DISEASES   OF   THE   HEART    AND    AORTA. 

are  comparatively  mild,  the  prognosis  is  a  little  better,  but  an  early  death 
from  phthisis  or  acute  endocarditis  is  always  to  be  feared,  even  when  the 
heart  failure  is  less  intense.  It  is,  therefore,  most  important,  as  Peacock 
suggested:  (1)  to  keep  the  patient  warm  by  both  warm  clothing  and 
sojourn  in  a  balmy  climate;  (2)  to  keep  him  leading  a  quiet  life  on  a  diet 
of  nourishing  but  easily  digested  food.  For  paroxysms  of  dyspnoea  and 
distress  free  purgation  should  be  resorted  to.  Venesection,  which  was  recom- 
mended by  Peacock,  though  indicated  by  both  the  venous  stasis  and  the 
high  viscosity  of  the  blood,  is  a  dangerous  procedure  and  should  be  used 
only  as  a  last  resort,  for  the  coagulation  of  the  blood  in  these  cases  is 
often  retarded.  Before  performing  it  the  coagulability  should  always  be 
determined. 

The  general  cardiac  stimulants,  such  as  digitalis  and  strychnine,  are 
rarely  of  much  value,  since  in  most  cases  the  heart  has  already  reached  the 
maximum  of  its  power  and  cannot  be  stimulated  much  further.  Vasodila- 
tion from  amyl  nitrite  and  nitroglycerin  may  sometimes  help,  and  Peacock 
recommends  the  use  of  warm  baths  or  mustard  baths,  especially  for  the 
convulsions  of  children. 


DEFECTS   IN   THE   INTERVENTRICULAR   SEPTUM. 
OCCURRENCE    AND    PATHOGENESIS. 

As  has  been  stated  above,  defects  in  the  interventricular  septum  are 
usually  with  and  secondary  to  other  malformations,  this  being  the  case  in 
117  (78  per  cent.)  of  149  cases  studied  by  Abbott.  Pulmonary  stenosis  or 
atresia  was  present  in  75  cases  (58  per  cent.).  In  only  24  cases  (16.1  per 
cent.)  were  there  no  other  abnormalities. 

The  circulatory  mechanism  which  keeps  the  septum  from  closing  in 
the  presence  of  pulmonary  stenosis  has  been  discussed  above  under  the 
latter  condition.  In  the  other  cases,  in  which  Abbott  classes  it  as  a  "  second- 
ary lesion,"  the  mechanism  is  similar. 

In  the  uncomplicated  cases,  however,  the  causation  is  more  obscure. 
In  a  few  cases  it  is  accounted  for  by  fetal  endocarditis  affecting  the  septum 
interpositum  before  the  septum  membranaceum  has  formed.  In  other 
cases  the  septum  membranaceum  does  not  form  completely.  After  birth, 
when  the  pressure  in  the  left  ventricle  rises  high  above  that  in  the  right, 
the  rush  of  blood  from  the  left  ventricle  into  the  right  may  push  the  septum 
along  with  it  and  may  cause  it  to  protrude  as  a  funnel  into  the  right  ven- 
tricle (Tate,  Hebb).  In  still  other  cases  the  septum  forms  and  protrudes  as 
an  aneurism  of  the  septum.  This  aneurism  may  rupture  later  and  give 
rise  to  the  defect. 

Some  cases  of  apparent  defect  in  the  septum  are  due  to  ulcerative 
septal  endocarditis,  but  these  are  probably  few.  Trauma  may  produce  a 
similar  effect  in  adult  life.  McOscar  and  Voelcker  report  the  case  of  a  man 
who  was  run  over  by  a  wagon.  Rupture  of  the  interventricular  septum 
resulted  and  the  patient  died  eight  days  afterwards.  Reiss  states  that 
pulmonary  tuberculosis  has  been  found  in  every  adult  in  his  series,  but  this 
is  by  no  means  always  the  case. 


CONGENITAL    HEART    DISEASE.  443 


PATHOLOGICAL    PHYSIOLOGY. 

When  the  defect  in  the  septum  is  secondary  to  a  severe  pulmonary- 
stenosis  or  atresia,  as  has  been  seen,  its  effect  is  to  allow  blood  to  pass  from 
the  right  ventricle  into  the  left,  and  under  any  circumstances  this  is  the 
case  during  fetal  life. 

When  there  is  no  such  stenosis,  however,  and  the  strength  of  the  left 
ventricle  increases  after  birth,  the  current  passes  in  the  reverse  direction 
and  aerated  blood  passes  from  the  left  ventricle  into  the  right.  The  effect 
upon  the  work  of  the  former  is  consequently  about  the  same  as  that  of  a 
leak  at  the  mitral  valve;  intraventricular  pressure  is  lowered,  and  the 
systolic  output  must  be  increased  in  order  to  maintain  the  circulation. 
The  left  ventricle  consequently  hypertrophies  as  a  result  of  the  strain;  the 
right  ventricle  hypertrophies  also  as  a  result  of  the  increase  in  the  blood 
forced  into  it.  The  extent  of  hypertrophy  of  the  latter  chamber  depends 
largely  upon  the  size  of  the  opening.  As  the  right  ventricle  hypertrophies 
and  pressure  in  the  right  ventricle  increases,  the  leakage  diminishes,  so 
that  the  effect  of  the  lesion  tends  to  correct  itself;  on  the  other  hand,  the 
pressure  in  the  pulmonary  artery  increases.  But  since  the  ordinary  resist- 
ance in  the  pulmonary  circulation  is  much  less  than  that  in  the  systemic, 
when  the  forces  of  both  ventricles  approximate  one  another,  the  effect  on 
the  pulmonary  circulation  is  the  same  as  though  the  left  ventricle  became 
weaker  and  the  right  remained  unchanged.  Pulmonary  engorgements 
may,  therefore,  result,  with  consequent  dyspnoea.  In  most  cases,  however, 
the  hypertrophy  does  not  reach  this  point,  and  it  is  only  when  the  heart  is 
stimulated  by  effort  or  exercise  that  pulmonary  engorgement  sets  in. 

SYMPTOMS. 

In  considering  the  symptoms  and  signs  of  defects  of  the  interventricular 
septum,  one  must  differentiate  sharply  between  those  cases  in  which  the 
condition  exists  alone  and  those  in  which  it  is  secondary  to  other  lesions. 
In  the  latter  case  the  manifestations  of  the  primary  condition  may  predomi- 
nate; and  these  are  discussed  in  the  corresponding  sections. 

The  symptoms  from  simple  defect  in  the  interventricular  septum  are 
few,  and,  as  a  rule,  are  confined  to  more  or  less  weakness,  dyspnoea,  and 
palpitation,  rather  than  the  extensive  symptom  complex  met  with  in 
pulmonary  stenosis. 

PHYSICAL    SIGNS. 

In  marked  contrast  to  pulmonary  stenosis,  marked  cyanosis  is  not 
one  of  the  signs  of  uncomplicated  defect  in  the  interventricular 
septum,  since  there  is,  as  a  rule,  no  stasis  in  the  veins  and  the  abnormal 
blood  stream  flows  from  left  ventricle  into  the  right.  Cyanosis  may  occur, 
however,  as  the  result  of  a  cardiac  overstrain,  just  as  in  any  other  condi- 
tion of  cardiac  weakness,  but  is  not  abnormally  intense.  The  fingers  are, 
as  a  rule,  not  clubbed.  Over  the  precordium  and  epigastrium  there  is 
usually  violent  systolic  retraction,  produced  by  the  hypertrophied  right 
ventricle.  There  may  be  violent  systolic  pulsation  of  the  conus  arteriosus 
in  the  second  left  interspace.    The  area  of  dulness  may  be  enlarged  to  both 


444 


DISEASES   OF   THE   HEART    AND    AORTA. 


right  and  left,  or  there  may  be  no  change  from  the  normal.  There  is 
almost  always  a  well-marked  systoUc  thrill  over  the  third  left  interspace 
near  the  sternal  margin. 

Auscultation  reveals  the  presence  of  a  murmur  which  was  first  described 
by  Roger  in  1879  in  the  following  words: 

"  It   is   in  general   remarkably   intense;   its   maximum   is   not   at   the   apex 
(as  in  alterations  of  the  auriculoventricular  orifices),  nor  at  the  right  base  (as  in  aortic 

stenosis),  nor  at  the  left  base  (as  in 
pulmonary  stenosis).  This  maximum 
is  at  the  upper  third  of  the  precor- 
dial region  and  is  median  like  the  ven- 
tricular septum  itself.  It  is  single 
and  very  prolonged,  commencing  with 
systole  and  replacing  the  two  normal 
sounds.  It  is  fixed  without  propa- 
gation in  the  large  vessels,  as  is  the 
case  with  aortic  or  pulmonary  stenosis, 
and  decreases  in  intensity  equally  in 
all  directions  as  one  passes  away  from 
this  central  point The  mur- 
mur corresponds  with  a  very  extensive 
thrill  which  exactly  coincides  with  it. 
....  The  murmur  does  not  change 
in  the  course  of  years." 

However,  all  writers  do  not 
agree  wdth  Roger.  Cadet  de 
Gassicourt,  Potain,  and  Reiss 
claim  that  it  occurs  during  systole  only;  while  in  some  cases,  especially  where 
the  septal  defect  is  a  large  one,  it  is  totally  absent  (Bennetz).  The  murmur 
is  sometimes  transmitted  to  the  carotid  arteries,  though  it  is  always  loud- 
est over  the  precordium.  The  second  pulmonary  sound  is  accentuated. 
The  pulse  may  be  small  and  weak,  or,  as  in  the  case  of  McOscar  and 
Voelcker,  collapsing.    The  blood-pressure  is  usually  low. 


Fig.  257. — Distribution  and  character  of  the  murmur  due 
to  a  patent  interventricular  septum  (Roger's  murmur). 


Case  of  Patent  Septum  Ventriculorum. 

The  following  notes  were  obtained  from  a  case  admitted  to  Prof.  Barker's  service 
in  the  private  wards  of  the  Johns  Hopkins  Hospital: 

The  patient  was  a  married  man,  a  scientist  of  some  note,  aged  59.  As  a  child  he  had 
been  subject  to  bad  dreams  and  disturbed  sleep  and  became  short  of  breath  on 
slight  exertion.  This  shortness  of  breath  on  exertion  followed  through  life,  but 
in  spite  of  the  ordinary  diseases  of  childhood,  three  mild  attacks  of  typhoid  fever,  and 
continued  use  of  tobacco,  alcohol,  and  strong  coffee,  he  was  able  to  lead  an  active  Hfe  until 
past  middle  age. 

For  six  weeks  before  admission  to  the  hospital  he  has  been  very  weak  and  has  been 
troubled  with  nocturnal  dyspnoea,  though  these  sj-mptoms  are  probably  refer- 
able to  his  renal  rather  than  to  his  cardiac  changes.  Swelling  of  the  feet  set  in  a  few  days 
before  admission. 

On  Feb.  15,  1908,  Dr.  Barker  made  the  following  note  on  his  cardiac  condition: 
The  radials  are  thickened,  the  blood-pressure  is  high;  there  is  a  blowing  systolic  murmur 
at  the  apex,  the  aortic  second  sound  is  fairly  loud,  the  pulmonic  second  very  loud.  The 
rough  systolic  murmur  is  also  heard  in  the  pulmonary  area, 
but  is  loudest  and  roughest  a  little  lateral  from  the  tricuspid 
area.  Xo  aortic  diastolic  murmur  is  heard.  There  is  no  marked  throbbing  of  the  neck; 
veins  in  the  neck  are  a  little  overfilled.  There  is  some  oedema  of  the  ankles  and  overfilling 
of  the  veins  of  the  lower  extremities. 


CONGENITAL   HEART    DISEASE.  445 

He  passed  over  2500  c.c.  of  urine  daily,  of  specific  gravity  1012-1014,  containing  a 
trace  of  albumen  and  some  hyaline  casts.  The  blood-pressure  varied  from  220  to  285 
mm.  Hg,  pulse-rate  80-90. 

During  his  stay  in  the  hospital  he  had  occasional  smothering  spells  which  were  relieved 
by  venesection.    He  spat  up  considerable  amounts  of  red  tenacious  sputum. 

The  patient  died  during  the  course  of  the  next  few  months.  Autopsy  revealed 
a  funnel-shaped  bulging  of  the  membranous  septum  into  the 
right  ventricle  with  a  perforation  3-4  mm.  in  diameter  at  the 
apex  of  the  funnel.  (This  condition  is  exactly  similar  to  the  lesion  described 
by  Hebb  and  by  Tate.) 

There  was  also  a  chronic  nephritis. 

C.\SE  OF  Probable  Patent  Septum  Vextriculorum. 

B.  J.,  an  unmarried  colored  woman  aged  26,  entered  the  Johns  Hopkins  Hospital 
complaining  of  pain  in  the  chest.  Except  for  shortness  of  breath  on  exertion  during  the 
last  ten  years,  the  history  is  negative. 

Her  heart  was  very  slightly  enlarged  to  the  right.  The  sounds  were  clear  at  the  apex, 
but  over  the  body  of  the  heart  a  peculiar  intense  high-pitched  murmur  was  heard,  loudest 
during  systole  but  lasting  through  the  whole  cardiac  cycle  (Roger's  murmur?).  This 
murmur  is  loudest  and  most  intense  over  the  third  left  interspace 
between  the  parasternal  line  and  the  sternum,  but  it  is  heard  also  in 
the  second  and  fourth  interspaces,  where  it  is  much  less  intense. 

Maximal  blood-pressure  varied  from  110  to  125  mm.  Hg;  venous  tracings  were  normal; 
retinal  vessels  normal.    The  urine  contained  a  trace  of  albumen  but  no  casts  nor  blood-cells. 

The  subsequent  history  was  uneventful. 

DIAGNOSIS. 

The  diagnosis  of  defect  in  the  interventricular  septum  can  be  made 
only  when,  in  the  absence  of  cyanosis  or  other  signs  of  congenital  heart 
disease,  the  vigorous  pulsation  of  the  right  ventricle  is  seen  in  the  second 
right  interspace,  and  both  the  peculiar  murmur  of  Roger  and  the  accent- 
uated second  pulmonic  sound  can  be  heard.  In  the  presence  of  pulmonary 
stenosis  or  other  congenital  or  acquired  lesions,  signs  may  merge  into  one 
another  in  such  a  way  that  an  absolute  diagnosis  may  be  impossible. 
Simple  acquired  endocarditis  often  occurs,  as  in  Tebb's  case,  and  its  signs 
may  serve  further  to  confuse  the  clinical  picture. 

TREATMENT. 

Needless  to  say,  there  is  no  treatment  that  can  be  directed  against 
the  defect  itself.  However,  the  symptoms  in  many  cases  arise  only  during 
over-exertion,  and  the  most  important  factor  in  the  management  of  the 
case  is,  therefore,  directed  along  the  usual  lines  for  the  avoidance  of  over- 
strain,— rest,  graduated  exercise,  moderation  in  diet,  avoidance  of  dyspnoea, 
regulation  of  the  bowels,  and  if  necessary  digitalis  and  strychnine.  The 
most  important  point  is  the  avoidance  of  pulmonary  congestion. 

The  PROGNOSIS  in  simple  septal  defect  depends  less  upon  the  extent 
of  the  lesion  than  upon  the  apparent  impairment  of  the  function.  Simple 
defects  in  the  septum  are  compatible  with  quite  long  life,  and  many  cases 
are  reported  in  which  the  patients  have  reached  the  fourth  and  fifth  decades. 

When  other  lesions  are  present,  such  as  pulmonary  stenosis,  abnormali- 
ties of  the  blood-vessels,  etc.,  it  is  they,  rather  than  the  septal  defect,  which 
determines  the  prognosis. 


446 


DISEASES   OF   THE   HEART    AND    AORTA. 


PATENT   FORAMEN   OVALE. 


OCCURRENCE    AND    PATHOGENESIS. 


Mere  patency  of  the  foramen  ovale  to  the  passage  of  a  probe  is  by  no 
means  pathological.  In  statistics  of  1166  heterogeneous  autopsies  collected 
by  Vierordt,  it  was  present  313  times  (28  per  cent.),  and  also  in  SO  (22.3  per 
cent.)  of  Zahn's  357  miscellaneous  <iutopsies  upon  persons  past  the  age  of 
40.  This  non-closure  is  probably  due  to  the  fact  that  both  the  auricular 
septum  and  the  valve  closing  the  foramen  are  lined  by  endothelium,  and 
no  fibrosis  takes  place  between  the  two  surfaces  until  the  endothelial  cells 
slough  off  or  are  injured.    The  valve  itself  remains  closed  against  the  septum 

during  life  and  no  symptoms  are 
produced.  Perhaps,  when  heart 
failure  from  any  cause  occurs  in 
such  cases  and  the  pressure  in  the 
right  auricle  exceeds  that  in  the 
left,  a  certain  amount  of  blood  may 
actually  pass  through  this  embryonic 
channel,  but  in  too  small  amounts 


RA      F^  LA 


Fig.  258. — Open  foramen  ovale.  (From  a  spec- 
imen in  the  Army  Medical  Museum,  Washington,  D. 
C. )  The  patient  was  a  soldier  who  had  never  shown 
any  cardiac  signs  or  symptoms  and  no  cyanosis. 


Fig.  259.  —  Diagram  showing  a  cross-section 
of  the  same.  VC,  vena  cava;  RA,  right  auricle; 
FO,  foramen  ovale;  LA,  left  auricle. 


to  give  signs  or  symptoms.  On  the  other  hand,  in  462  autopsies  by  Hinze 
and  by  Ogle  the  foramen  was  permeable  to  the  little  finger  (permanently 
patent)  in  only  9  cases  (1.9  per  cent.). 

The  mechanism  of  secondary  septal  defects  (auricular  stasis  of  Mor- 
gagni  and  William  Hunter)  by  which  more  than  the  usual  proportion  of 
blood  passes  through  the  foramen  ovale  has  been  discussed  under  pulmo- 
nary stenosis,  and  it  may  occur  with  other  congenital  lesions. 

The  truly  pathological  lesions  of  the  interauricular  septum  are  shrink- 
age or  total  absence  of  the  valve  and  perforation  of  the  septum  between 
the  muscle  strands  (Fig.  260).  Occasionally  the  valve  has  closed,  but  is 
somewhat  weak  and  forms  an  aneurismal  bulging.  Peacock  reports  one 
and  Abbott  two  of  these  cases,  in  all  of  which  the  protrusion  was  from  right 
to  left,  indicating  that  the  pressure  in  the  right  ventricle  exceeded  that  in 
the  left. 


CONGENITAL   HEART    DISEASE. 


447 


Valv.F.O 


PATHOLOGICAL    PHYSIOLOGY. 

A  defect  in  the  interauricular  septum  has  comparatively  little  effect 
upon  the  circulation  as  long  as  the  pressures  in  the  two  auricles  are  equal 
or  nearly  so.  When  the  left  ventricle  begins  to  fail  or  the  pressure  in  the 
left  auricle  rises  from  any  cause  whatever  (mitral  stenosis,  mitral  insuffi- 
ciency, etc.),  the  patent  foramen  ovale  exercises  a  sort  of  safety-valve  action 
and  relieves  the  pulmonary  congestion  by  allowing  the  excess  of  blood  to 
pass  back  into  the  right  auricle.  Ritter  (1856)  and  Rusch  (1862)  have 
shown  that  when  the  foramen  ovale  is  open  in  cases  of  mitral  insuf- 
ficiency, the  pulsation  in  the  jugular  vein  assumes  the  positive  ven- 
tricular type,  owing  to  the  crossing  of  the  regurgitant  stream.  How- 
ever, this  is  of  little  value  in  .diagnosis,  since  the  positive  ventricular 
pulse  is  common  with  heart  weakness 
and   auricular  paralysis. 

On  the  other  hand,  when  the  right 
heart  begins  to  fail  and  pressure  in  the 
left  auricle  increases,  the  blood  follow^s 
the  same  course  as  it  does  in  the  foetus 
and  passes  from  the  right  into  the  left  fokamin 
auricle.  Under  ordinary  circumstances 
this  would  exert  no  influence  whatever, 
and  would  not  even  produce  cyanosis. 
But  when  the  heart  is  already  weak,  the 
circulation  slow,  and  the  blood  heavily 
charged  with  COj,  this  sudden  admixture 
of  venous  blood  carries  the  CO2  content 
past  the  physiological  limit,  and  gives 
rise  to  cyanosis  and  symptoms.  More- 
over, the  blood  entering  the  coronary 
arteries  is  also  less  aerated,  the  cardiac 
tonicity  and  cardiac  strength  are  im- 
paired, and  the  vicious  circle  of  the  open 
foramen  ovale  sets  in,  subsiding  again  wdth  inordinate  rapidity  as  soon 
as  the  pressure  in  the  systemic  veins  falls  below  that  in  the  pulmonary. 


Fig.  260. — Openings  between  strands  ot 
muscle  in  the  interauricular  septum.  (From 
a  specimen  in  the  Army  Medical  Museum, 
Washington,  D.  C.)  The  valvula  foraminis 
ovalis  {VALV.  F.O.)  is  closed  and  has  fusefl 
with  the  rest  of  the  septum.  FORAMINA, 
abnormal  openings  between  strands  of  mus- 
cle in  the  lower  part  of  the  septum. 


SYMPTOMS. 

In  most  cases  patency  of  the  foramen  ovale  alone  does  not  give  rise 
to  any  symptoms.  For  example,  the  patient  whose  heart  is  shown  in  Fig. 
237  was  able  to  perform  his  duties  as  a  soldier  in  heavy  campaigns  and 
died  from  dysentery  without  any  symptoms  referable  to  his  heart.  Pea- 
cock mentions  the  case,  reported  by  Spry  in  1805,  of  a  girl  of  seven  years 
who  had  no  cyanosis  during  life  and  whose  foramen  was  patent  and  two 
inches  in  circumference  (f  inch  in  diameter).  On  the  other  hand,  he  cites 
another  case,  a  woman  of  twenty-one  whose  foramen  ovale  was  one  inch 
in  diameter,  who  from  the  age  of  three  months  "presented  characteristic 
symptoms  of  malformation  of  the  heart, — cyanosis,  palpitation,  dyspnoea, 
faintings,  occasional  convulsive  attacks,  and  lividity." 


448  DISEASES   OF   THE    HEART    AND    AORTA. 


PHYSICAL    SIGNS. 

Apart  from  the  paroxysmal  cyanosis  the  physical  signs  of  open  fora- 
men ovale  are  extremely  variable.  Cyanosis  and  abnormalities  in  the  retina 
may  be  present.  On  the  other  hand,  all  physical  signs  may  be  absent.  In 
some  cases  systolic,  in  others  diastolic,  murmurs  are  present  in  the  third 
left  interspace  at  the  sternal  margin.  Occasionally  there  is  heard  a  well- 
defined  presystolic  murmur  which  is  maximal  at  this  point,  and  which 
when  present  is  the  most  characteristic  sign  of  the  open  foramen  ovale. 

DI.\GNOSIS. 

The  diagnosis  rests  upon  the  presence  of  paroxysmal  cyanosis 
and  of  murmurs  in  the  third  left  interspace  without  signs 
of  aortic  insufficiency  or  of  hypertrophy  of  the  right  ventricle  (well-marked 
systolic  retraction  over  the  right  ventricle  with  or  without  systolic  impulse 
in  the  second  left  interspace)  or  of  other  congenital  heart  lesions.  This  is 
especially  corroborated  if  the  child  was  a  blue  baby  at  birth  or  within  a 
few  months  afterwards,  even  if  only  during  intervals  of  a  few  hours  or  days. 
The  retinal  changes  are  valuable  signs  when  present. 

In  rare  cases  incidental  phenomena  may  help  in  the  diagnosis.  Cohnheim  cites  a 
case  in  which  the  diagnosis  was  made  from  the  occurrence  of  embolism  of  the  brain  when 
the  primary  thrombus  was  in  the  veins  of  the  leg  (crossed  embolism);  but  such  cases  are 
necessarily  extremely  rare,  and  before  such  inferences  are  made  all  commoner  factors  must 
be  carefully  excluded. 

TREATMENT. 

Treatment  between  attacks  of  cyanosis  and  dyspnoea  is  confined  to 
general  hygiene  and  regulation  of  the  patient's  life,  as  described  above  for 
pulmonary  stenosis,  though,  as  a  rule,  more  latitude  may  be  allowed. 

During  the  attacks  hot  baths  and  vasodilators  (such  as 
amyl  nitrite  and  nitroglycerin)  may  be  resorted  to,  and,  when  there  is  no 
diminished  coagulability  and  the  attack  is  severe,  venesection  may  be 
performed. 

PATENT   DUCTUS   ARTERIOSUS    (BOTALLI). 
PATHOGENESIS.- 

In  many  cases  in  which  the  arterial  circulation  is  markedly  disturbed 
in  the  foetus,  the  ductus  arteriosus  (Botalli)  may  be  found  to  remain  patent 
after  birth.  This  is  a  common  concomitant  of  pulmonary  stenosis  and 
especially  pulmonary  atresia,  of  the  corresponding  conditions  at  the  aortic 
orifice,  and  of  congenital  lesions  at  either  of  the  auriculoventricular  valves. 

When  viewed  in  the  light  of  its  closure,  the  mechanism  of  this  secondary 
non-closure  of  the  ductus  is  tolerably  clear.  The  ductus  arteriosus  Botalli 
represents  the  remains  of  the  sixth  branchial  arch  (Fig.  240).  It  "is  in 
a  direct  line  with  the  pulmonary  trunk,  is  the  direct  continuation  of  the 
same,  and  is  of  almost  equal  size,  while  it  is  of  greater  diameter  than  the 
descending  arch  of  the  aorta.  A  distinct  narrowing  of  the  aortic  arch  is 
to  be  observed  just  above  the  entrance  of  the  ductus  into  it."    (Klotz.) 


CONGENITAL   HEART   DISEASE.  449 

Closure  of  the  Ductus  Arteriosus. — Several  theories  have  been  advanced 
to  explain  the  closure  of  the  ductus  arteriosus  at  birth: 

Haller  thought  that  it  results  from  coagulation  of  the  blood  within  its  lumen.  Kiliani 
(1826)  was  the  first  to  show  that  with  the  expansion  of  the  lungs  at  birth  the  resistance 
in  the  pulmonary  circulation  was  diminished  and  a  large  amount  of  blood  thus  diverted 
from  the  channel  through  the  ductus.  A  number  of  theories  have  been  proposed  to  explain 
the  exact  manner  in  which  this  diversion  of  blood  through  the  pulmonary  channels  brings 
about  the  closure  of  the  ductus  arteriosus. 

Strassman  (1894)  attempted  to  explain  the  closure  on  purely  mechanical  grounds. 
He  called  attention  to  the  fact  that  the  ductus  arteriosus  penetrates  the  wall  of  the  aorta 
at  an  acute  angle,  so  that  the  tissue  included  in  this  angle  forms  a  sort  of  valve.  He 
believed  that  when  the  pressure  within  the  aorta  became  greater  than  that  in  the  pulmonary 
artery  (after  birth),  this  flap  of  vessel  wall  closed  down  over  the  mouth  of  the  ductus  and 
prevented  blood  from  entering  it.  Strassman  found,  moreover,  that  if  he  injected  fluid 
into  the  aorta  of  a  new-born  child  at  a  pressure  under  100  mm.  no  blood  entered  the  pul- 
monary artery.  These  exjjeriments  have  been  very  carefully  repeated  in  a  large  number 
of  infants  by  Klotz,  who  found  that  "at  all  times  when  the  ductus  arteriosus  was  unob- 
literated  by  new-formed  or  forming  fibrous  tissue  the  colored  fluid  found  its  way  into  it 
for  some  distance  sufficient  to  stain  it."  However,  the  fact  that  the  communication  was 
not  a  free  one  demonstrates  that  this  valvular  action  is  probably  a  contributing  cause  in 
cutting  off  the  blood  flow  or  in  lessening  the  pressure  in  the  ductus. 

On  the  other  hand,  Schulze  in  1871  showed  that  the  walls  of  the  ductus  arteriosus, 
though  poor  in  or  lacking  elastic  fibres,  were  particularly  rich  in  muscle  fibres.  He  believed 
that  when  the  blood-pressure  in  the  pulmonary  artery  fell,  and  the  blood  was  diverted 
away  from  the  ductus  arteriosus,  the  muscle  fibres  in  the  wall  contracted  down  further 
until  the  lumen  was  finally  obliterated.  This  occurs  without  any  such  intravascular  co- 
agulation as  Haller  had  supposed;  but  Langer  (1857)  has  found  that  it  is  accompanied 
by  a  very  active  proliferation  of  the  cells  in  the  intima,  with  sloughing  off  of  the  endothelial 
lining  (Klotz).  The  proliferation  goes  on  till  the  wall  of  the  vessel  becomes  thicker  than 
that  of  either  the  pulmonary  artery  or  the  aorta,  and  it  is  finally  occluded  by  fibrosis. 

Factors  Causing  Persistence  of  Ductus. — Under  pathological  conditions 
it  is  clear  that  anything  which  causes  obstruction  to  the  flow  of  blood 
through  the  arch  of  the  aorta  during  fetal  life  (aortic  stenosis  or  atresia, 
congenital  mitral  stenosis,  coarctation  of  the  arch  of  the  aorta,  etc.)  will 
cause  the  right  ventricle  to  carry  on  the  greater  part  of  the  circulation  and 
to  force  more  blood  than  usual  through  the  ductus  arteriosus.  This  condi- 
tion, of  course,  persists  after  birth;  the  ductus,  which  now  represents  a 
main  blood  channel,  remains  open.  The  flow  continues  in  the  usual  direc- 
tion backward  from  the  pulmonary  artery  into  the  aorta. 

On  the  other  hand,  when  there  is  atresia  of  the  pulmonary  artery  the 
pressure  in  the  ductus  is  low  and  blood  enters  it  from  the  aorta,  passing 
f  o  w  a  r  d  (ventrally)  into  the  rami  pulmonales.  These  facts  explain  the 
persistence  of  the  ductus  arteriosus  in  its  usual  occurrence  as  a  secondary 
congenital  lesion. 

The  occurrence  as  a  primary  lesion  is  rare,  only  26  cases  having  been 
collected  by  Vierordt  in  1898,  12  more  by  Abbott.  Klotz  believes  that 
these  may  be  "the  result  of  imperfect  expansion  of  the  lungs.  In  these 
cases  the  blood-pressure  has  never  been  lowered  in  the  pulmonary  system 
to  the  point  which  allowed  the  walls  of  the  ductus  to  overcome  it."  It 
may  also  result  from  congenital  weakness  of  the  left  ventricle  causing  a 
low  blood-pressure  in  the  aorta  at  the  time  of  birth. 

The  size  and  structure  of  the  patent  ductus  may  vary  greatly,  from  a 
short  and  narrow  passage  to  an  almost  aneurismal  dilatation.  Acute  or 
29 


450  DISEASES   OF   THE   HEART   AND    AORTA. 

malignant  vegetations  are  not  uncommon  within  the  lumen,  and  the  pres- 
ence of  an  open  ductus  tends  to  predispose  to  endocarditis.  Arterioscle- 
rosis of  both  the  ductus  and  the  pulmonary  artery  also  occurs,  perhaps  as 
a  result  of  the  high  pulmonary  pressure. 

SYMPTOMS. 

The  symptoms  of  uncomplicated  patent  ductus  arteriosus  are  usually 
obscure  and  slight,  and  the  condition  is  often  found  incidentally.  Cyano- 
sis is  slight  and  transitory.  Slight  weakness  and  shortness  of  breath  on 
exertion  may  occur,  but  many  of  the  cases  are  devoid  of  symptoms. 

PHYSICAL    SIGNS. 

Several  diagnostic  features  of  open  ductus  arteriosus  have  been  pub- 
lished at  various  times.  Gerhardt  in  1867  described  a  small  quadrilateral 
extension  of  the  area  of  dulness  in  the  second  (and  first) 
left  interspace.  In  this  region  the  pulsation  of  the  pulmonary  artery  may 
be  seen,  and  the  well-marked  systolic  retraction  is  often  seen  over  the  inter- 
spaces corresponding  to  the  hypertrophied  right  ventricle.  Zinn,  de  la 
Camp,  and  others  have  found,  on  examination  with  the  fluoroscope,  that 
Gerhardt's  area  of  dulness  corresponds  to  a  round  shadow  of  a 
small  mass  along  the  left  upper  margin  of  the  cardiac  shadow,  where 
the  pulmonary  artery  and  left  auricle  are  usually  seen  (Fig.  261) .  This 
mass  shows  systolic  pulsation  and  corresponds  to  the  dilated  ductus  arterio- 
sus. This  dilatation  is  frequently  aneurismal.  The  picture  with  the  X-ray 
is  thus  of  great  diagnostic  value,  but  one  must  carefully  exclude  an  aneu- 
rism of  the  aorta  behind  the  sinus  of  Valsalva.  In  contrast  to  the  shadow 
of  the  left  auricle,  this  shadow  is  magnified  when  the  tube  is  placed  in  front 
of  the  body  as  compared  with  the  illumination  from  behind. 

The  signs  on  auscultation  vary  considerably.  There  is  usually 
a  systolic  murmur  over  the  precordium,  and  especially  over  the 
second  left  interspace,  which  sometimes  replaces  but  often  follows  the  first 
sound.  This  murmur  when  not  caused  by  another  concomitant  lesion  is 
due  to  the  rush  of  blood  through  a  narrowed  ductus  into  the  wider  lumen 
of  the  aorta.  Fran^ois-Franck  has  shown  that  this  murmur  is 
heard  loudly  at  the  left  back  over  the  area  at  which  the  aorta 
comes  in  contact  with  the  chest  wall  (level  of  the  third  and  fourth  spines), 
to  which  it  is  transmitted  in  a  direct  line  (Fig.  256).  He  showed  that 
the  loudness  of  this  murmur  bears  a  definite  relation  to  the  phases  of  respi- 
ration. It  is  loudest  during  expiration,  for  at  that  time  the  resistance  in 
the  pulmonary  circuit  is  greatest,  and  hence  the  blood  flows  through  the 
ductus  more  rapidly;  but  becomes  feebler  in  inspiration  when  more 
blood  passes  through  the  lungs  and  less  through  the  ductus.  Fran^ois- 
P>anck  also  found  that  this  variation  in  the  blood  flow  into  the  aorta 
found  equally  marked  expression  in  the  pulse,  causing  a  rise  of  pressure 
and  full  pulse  in  expiration,  fall  and  small  pulse  during  inspiration 
(pulsus  paradoxus). 

These  signs,  however,  occur  only  in  cases  in  which  there  is  an  efficient 
circulation  through  the  pulmonary  orifice.     In  the  cases  associated  with 


CONGENITAL   HEART    DISEASE. 


451 


pulmonary  atresia  where  the  flow  through  the  ductus  is  in  the  opposite 
direction,  the  murmur  may  be  absent  at  the  back  and  will  be  loudest  during 
inspiration,  for  then  the  inflow  into  the  lungs  is  greatest.  Never- 
theless, the  pulse  will  remain  a  pulsus  paradoxus,  for  the  flow 
through  the  aorta  during  inspiration  will  be  diminished  just  the  same. 
This  respiratory  variation  of  murmur  and  pulse  is,  however, 
often  absent  in  spite  of  the  open  ductus,  as  is  the  systolic  murmur  itself 
in  some  cases.  Neither  bears  an  absolute  relation  to  the  degree  of  patency 
of  the  ductus. 


DB 


MI 


Fui.  261. — Radiograpli  of  a  thirteen-year-old  boy  with  patent  ductus  arteriosus  (Botalli)  and  aneu- 
rismal  dilatation  of  the  ductus  and  pulmonary  artery.  (After  Hochsinger,  in  Pfaundler  and  Schlossmann's 
•'Diseases  of  Children.")  AA,  arch  of  the  aorta;  DB,  ductus  Botalli  and  pulmonary  artery  dilateti  like 
an  aneurism,  giving  a  cap-shaped  top  to  the  shadow  of  the  heart;  MI,  internal  mammary  artery,  consider- 
ably dilated,  denoting  an  internal  collateral  circulation. 


A  diastolic  murmur  is  often  heard  along  with  the  systolic,  sometimes 
replacing  the  second  sound  but  more  often  accompanying  or  following  an 
accentuated  pulmonic  sound.  The  inequality  in  pressure  between  aorta 
and  pulmonary  artery  persists  during  diastole,  and  the  abnormal  blood 
flow  therefore  continues  and  produces  the  murmur  in  diastole.  When  the 
difference  of  pressure  is  slight,  especially  with  low  peripheral  resistance, 
the  diastolic  murmur  may  be  absent. 


452  -     DISEASES   OF  THE   HEART   AND    AORTA. 

DIAGNOSIS. 

From  the  above  discussion  the  points  upon  which  the  diagnosis  of  the 
open  ductus  arteriosus  may  rest  are  sufficiently  clear, — pulsation  over  the 
right  ventricle,  Gerhardt's  dulness,  a  systolic  or  double  murmur  loudest  at 
second  left  interspace  and  heard  at  the  left  upper  back,  expiratory  accent- 
uation and  pulsus  paradoxus,  and  the  pulsating  mass  in  Gerhardt's  area 
seen  on  X-ray  examination.  In  addition,  the  history  may  show  that  the 
patient  was  blue  at  birth  (before  the  pulmonary  channels  have  opened  up) 
but  that  cyanosis  soon  passed  off. 

J.  Plesch  in  Kraus's  clinic  (Berl.  klin.  Wchnschr.,  1909,  xlvi,  391)  has  attempted 
to  make  the  diagnosis  by  analyses  of  the  expired  air.  By  a  very  simple  device  he  deter- 
mines the  percentage  to  which  the  blood  flowing  through  the  pulmonary  artery  is  satu- 
rated with  oxygen.  Under  normal  conditions  the  saturation  is  38-70  per  cent,  of  its  oxygen 
capacity.  In  patent  ductus  arteriosus  the  blood  in  the  pulmonary  artery  is  mixed  blood 
and  hence  its  oxygen  content  is  higher  (80-90  per  cent.).  The  aerated  blood 
could  enter  only  through  a  patent  ductus  arteriosus. 

TREATMENT. 

Treatment  for  the  persistence  of  the  ductus  consists  mainly  in  those 
methods  which  improve  pulmonary  circulation, — breathing  exercises, 
careful  hygiene,  avoidance  of  exposure  to  pulmonary  infections,  and  avoid- 
ance of  fatigue,  general  muscular  and  cardiac  overstrain.  Since  the  per- 
sistence of  the  ductus  is  in  itself  a  compensatory  process,  it  calls  for  no 
special  remedy.  To  ligate  it,  as  might  readily  be  done  after  opening  up 
the  thorax  under  positive  pressure,  would  be  harmful  rather  than  bene- 
ficial. Otherwise  general  hygienic  measures  and  cardiac  stimulants  are 
of  value,  as  in  other  diseases.  But  in  many  cases  open  ductus  Botalli  has 
no  effect  upon  the  duration  of  life  and  requires  no  treatment. 

STENOSIS    OF   THE   AORTA. 

Stenosis  of  the  lumen  of  the  aorta  may  occur  in  three  places: 
I.  At  the  aortic  valve. 
II.  Stenosis  of  the  arch  of  the  aorta. 

1.  Above  the  entrance  of  the  ductus  arteriosus  Botalli. 

2.  Just  below  the  entrance  of  the  ductus  arteriosus  Botalli. 

I.  Stenosis  at  the  aortic  orifice  is  one  of  the  rarer  con- 
genital lesions  (2  per  cent,  of  Abbott's  series),  though  probably  many  of 
the  milder  cases  escape  detection.  It  is  usually  due  to  endocarditis  late  in 
fetal  life. 

Those  which  develop  earlier  in  fetal  existence,  in  which  true  aortic 
atresia  occurs,  are  quite  analogous  to  the  cases  of  pulmonary  atresia, 
except  that  the  posterior  instead  of  the  anterior  channel  of  the  common 
truncus  arteriosus  fails  to  develop.  The  changes  in  the  fetal  circulation 
are  similar  to  those  in  pulmonary  atresia,  but  affect  the  opposite  sides  of 
the  heart.  The  septa  remain  open,  and  occasionally  one  ventricle  (the  left) 
fails  to  develop.  Practically  the  entire  systemic  circulation  is  carried  on 
by  the  pulmonary  artery  through  the  ductus  arteriosus. 

The  consequences  of  the  lesion  are  very  severe  and  few  cases  survive 
birth,  in  striking  contrast  to  pulmonary  stenosis  and  atresia.     No  doubt 


CONGENITAL   HEART   DISEASE.  453 

this  is  due  to  the  fact  that,  since  the  right  ventricle  is  the  stronger  in  fetal 
life,  it  succeeds  in  establishing  a  better  compensatory  circulation  after 
atresia  of  its  orifice  than  does  the  left.  Moreover,  when  the  first  breath  is 
taken  after  stenosis  of  the  aorta,  it  is  venous  instead  of  arterial  blood 
which  is  thrown  into  the  organs. 

11.  Stenosis  in  the  vicinity  of  the  ductus  Botalli 
is  one  of  the  most  common  congenital  heart  lesions,  occurring  in  198  of 
Abbott's  412  cases.  Like  most  abnormalities  it  arises  as  an  exaggeration 
of  a  condition  which  is  normally  present  in  the  foetus.  As  stated  above, 
Klotz  finds  that  there  is  a  distinct  narrowing  of  the  aortic  arch  just  above 
the  entrance  of  the  ductus  into  it.  This  is  no  doubt  due  to  the  fall  of  pres- 
sure in  the  aorta  which  occurs  below  the  left  carotid  artery  and  the  rise 
further  on  when  the  blood  enters  from  the  ductus. 

Hamernik  in  1844  divided  the  cases  into:  (1)  stenosis  above  the 
ductus,  (2)  those  at  the  entrance  of  the  ductus,  and  (3)  those  below  the 
ductus.  Bonnet,  who  made  an  exhaustive  study  of  the  subject  in  1903, 
discards  Hamernik's  second  group,  and  distinguishes  two  types: 

1.  The  type  in  the  new-born,  in  which  the  stenosis  occurs  above  the 

ductus  and  the  latter  remains  open. 

2.  The  type  found  in  adults,  in  which  the  stenosis  occurs  below  the 

ductus.    The  latter  is  closed  and  collateral  circulation  develops. 

Bonnet's  studies  were  based  upon  160  cases,  of  which  55  (34.3  per  cent.) 
were  of  the  new-born  type  and  105  (65.7  per  cent.)  were  of  the  adult  type. 

Type  of  the  New=born. — The  cases  of  the  new-born  type  represent  an 
exaggeration  of  the  slight  narrowing  in  the  aorta  which,  as  Klotz  states, 
is  present  above  the  left  subclavian  artery  and  the  ductus  Botalli.  Em- 
bryologically,  as  Longa  points  out,  this  represents  the  branch 
joining  the  fourth  and  sixth 
branchial  arteries  (Fig.  240) 
and  might  correspond  to  a  failure  of 
development  of  this  branch.  On  the 
other  hand,  the  amount  of  blood  in  the 
,  aorta  is  very  much  depleted  by  the 
flow  into  the  innominate,  left  carotid, 
and  subclavian,  so  that  its  lumen  is 
naturally  smaller  until  replenished  by 
the  inflow  from  the  ductus.  There  is 
consequently  a  region  of  functional 
stenosis  between  these  two  points 
which  may  be  exaggerated  by  con- 
traction of  the  muscle-fibres  in  the  pio.  262.— stenosis  of  the  isthmus  of  the 
wall  of  the  aorta.  The  weaker  the  ^orta  above  the  ductus  arteriosus  (Botalli)  - 
.11  type  of  the  new-born.  (From  a  specimen  m  the 
action   of    the    left    ventricle    the    more        Army  Medical  Museum,  Washington,  D.  C.) 

marked  will  be  this  functional  steno- 
sis. The  ductus  Botalli  therefore  takes  on  more  and  more  of  the  circu- 
lation in  the  lower  parts  of  the  body,  and  fetal  life  may  be  undisturbed  as 
long  as  the  right  ventricle  is  pumping  aerated  blood ;  but  when  this  con- 
dition ceases  and  the  pulmonary  channels  widen  and  pressure  in  the  ductus 
falls,  the  aortic  circulation  may  become  insufficient  and  the  syndrome  of 


454 


DISEASES   OF   THE    HEART    AND    AORTA. 


congenital  heart  disease  ma}'  result.  It  is  rare  for  these  children  to  live 
more  than  a  few  weeks,  or  at  most  a  few  months,  and  many  die  at  birth. 
Physical  signs  are  indefinite,  confined  to  double  murmurs  over 
the  chest  and  back  and  in  most  cases  cyanosis.  There  are  very  often  asso- 
ciated malformations,  such  as  pulmonary  stenosis,  open  septum  ventric- 
uloium,  etc. 

In  this  form  there  is  very  little  attempt  at  establishment  of  a  c  o  1 1  a  t- 
e  r  a  1  circulation,  since  the  greater  part  of  the  systemic  circulation 
is  maintained  by  the  right  ventricle  through  the  open  ductus  arteriosus, 
just  as  it  is  before  birth.  Owing  to  the  completeness  of  this  compensation, 
there  may  be  little  difference  between  the  pulses  in  the  upper  and  in  the 
lower  extremities,  and  the  clinical  diagnosis  is  scarcely  ever  made. 

Adult  Type.  —  In  the  second  or  adult  type,  which  is  more 
common,  the  stenosis  occurs  just  below  the  entrance  of  the  ductus  Botalli, 
and  this  vessel  is  found  to  be  closed.     Indeed,  the  very  stasis  at  this  point 

assists  in  its  closure.  The  mode  of 
origin  of  the  stenosis  at  this  point  is 
not  clear.  Bonnet  calls  attention  to 
the  fact  that  the  lumen  of  the  aorta 
at  the  stenosis  (usually  2-4  mm.)  is 
about  that  of  the  normal  aorta  at  the 
time  of  birth,  and  thinks  that  the 
whole  anomaly  may  be  of  post- 
natal development.  It  is  possible, 
as  he  suggests,  that,  when  the  ductus 
Botalli  is  particularly  long,  the  fibro- 
sis of  the  latter  brings  about  a  kink- 
ing of  the  aorta  at  this  point,  and 
with  a  dilatation  above  and  stenosis 
at  the  point  of  kinking. 

Skoda,  on  the  other  hand,  has 

suggested    that    the    stenosis    may 

result  from  a  band  of  fibrosis  passing 

around  the  aorta  at  this  point;  but,  though  this  theory  is  alluring,  there 

is  no  definite  histological  evidence  in  its  support. 

The  stenosis  cuts  off  the  circulation  from  all  parts  of  the  body  below 
the  stenosis,  but  the  high  pressure  due  to  the  stagnation  above  it  causes  a 
progressive  dilatation  of  other  arterial  channels,  such  as  the  mammaries, 
thoracic  and  scapular  arteries,  which  are  always  found  to  be  much  dilated. 
Indeed,  the  collateral  circulation  may  be  so  good  that  the  lumen  of  the  aorta 
below  the  stenosis  may  be  as  great  as  above  it  (hour-glass  constriction), 
though  usually  it  is  somewhat  narrow"'and  it  may  even  be  funnel-shaped. 
CUnically  the  presence  of  this  type  of  stenosis  does  not  necessarily 
shorten  life,  though  this  depends  largely  upon  the  completeness  of  the 
collateral  circulation.  The  symptoms  are  chiefly  those  of  cerebral  conges- 
tion,—headache,  vertigo,  buzzing  in  the  ears.  Occasionally  there  are  pains 
in  the  chest.  Bonnet  calls  attention  to  the  fact  that  in  his  105  cases  there 
was  never  intermittent  claudication,  showing  that  the  circulation  in  the 
lower  limbs  is  always  sufficient. 


Fig.  263. — Stenosis  below  the  ductus  arteri 
osus  (Botalli). — adult  type.  (Aft«r  Bonnet,  Rev 
de  Mod.,  Par.,  1903,  xxiii.) 


CONGENITAL   HEART    DISEASE.  455 


PHYSICAL    SIGNS    AND    DIAGNOSIS. 

Cyanosis  is  not  common  and  not  a  sign  of  the  disease.  The  most 
definite  indication  is  the  difference  in  the  size  and  quality  of  the  pulse  in 
the  upper  and  lower  extremities,  the  carotid  and  radial  pulses  being  large 
and  throbbing,  the  femoral,  popliteal,  and  dorsalis  pedis  as  well  as  the 
abdominal  aorta  small  or  impalpable.  Though  the  diagnosis  intra  vitam 
is  rare,  Lepine  was  able  to  make  it  from  these  data  in  two  cases.  Dr.  W.  S. 
Morrow  calls  attention  to  the  possibility  of  diagnosis  from  marked  differ- 
ence in  the  brachial  and  tibial  blood-pressures,  but  just  as  in  aneurisms 
the  difference  in  size  and  quality  of  the  pulse  on  palpation  would  usually 
be  more  marked  than  that  of  the  blood-pressures.  Moreover,  Halsted 
has  found  little  difference  between  brachial  and  femoral  pressures  in  man 
after  the  abdominal  aorta  has  been  occluded  with  metal  bands  for  the  treat- 
ment of  aneurism.  The  presence  of  large  tortuous  mammary,  thoracic, 
and  scapular  arteries  aids  in  the  diagnosis.  There  are  usually  low  murmurs 
over  the  arteries,  especially  at  the  angle  of  the  left  scapula,  as  was  present 
in  a  case  diagnosed  by  Mercier  in  1839. 

Valvular  disease  of  the  heart  frequently  results  from  the  increased 
work  thrown  upon  the  heart  and  dilatation  of  aortic  and  mitral  orifices, 
and  their  signs  complicate  the  picture.  Before  making  the  diagnosis,  it  is 
alwaj's  necessary  to  exclude  aneurism  and  mediastinal  tumor  by  the  absence 
of  dulness  on  percussion  and  of  abnormal  shadows  on  X-ray  examination. 

TREATMENT. 

Treatment  depends  purely  upon  symptoms,  occasional  venesection 
being  of  value  to  relieve  the  headaches.  It  is  most  important  for  the 
patient  who  suffers  from  these  symptoms  to  avoid  over-exertion  or  excite- 
ment, which  cause  too  vigorous  action  of  the  heart. 

DIFFUSE    NARROWING    OF    THE    AORTA. 

Virchow  has  also  called  attention  to  another  form  of  abnormality  in 
the  lumen  of  the  aorta,  a  diffuse  narrowing  of  its  entire  lumen  throughout 
its  whole  extent  (hypoplasia  of  the  aorta).  This  condition  is  associated 
with  under-development  of  the  elastic  and  muscular  elements  in  the  arterial 
walls.  As  Virchow  and  other  observers  have  found,  it  is  often  associated 
Avith  chlorosis  of  intense  grades  and  occasionally  accompanies  other  con- 
genital malformations  of  the  heart. 

About  the  objective  finding  there  is  little  dispute.  The  only  point  in 
question  is  whether  the  condition  is  to  be  regarded  as  a  true  congenital 
malformation  or  as  a  postnatal  development,  which,  like  the  changes  in 
rickets,  is  determined  by  conditions  of  growth  and  nutrition  during  child- 
hood and  may  be  corrected  by  cure  of  these  conditions.  It  is  possible  that 
it  may  be  secondary  to  the  conditions  which  bring  on  anaemia,  and  due  to 
the  fact  that  the  aortic  walls  have  never  been  subjected  to  the  stimulating 
influence  of  an  adequately  high  blood-pressure.  That  this  may  be  a  factor 
in  the  development  of  and  strengthening  of  blood-vessel  walls  has  been 
shown  especially  by  the  results  of  arteriovenous  anastomosis  and  trans- 


456 


.    DISEASES   OF   THE    HEART    AND    AORTA. 


plantation,  in  which  the  walls  of  the  transplanted  vein  become  thicker  and 
richer  in  elastic  and  muscular  elements  (Carrel).  It  is  of  course  extremely 
difficult  to  determine  what  would  have  occurred  if  such  cases  had  recovered 
from  their  anemia  or  primary  debility  and  blood-pressure  had  reached  a 
normal  level.  It  is  equally  difficult  to  determine  that  any  such  cases  have 
recovered  under  these  conditions,  though  the  fact  that  the  lumen  of  the 
radial  artery  increases  (pulse  becomes  larger)  with  the  recovery  from 
chlorosis  is  of  course  definite. 

For  the  present,  therefore,  one  must  hesitate  somewhat  in  classing 
hypoplasia  of  the  aorta  among  the  definite  congenital  malformations. 


Fic;.264. — Transposition  of  the  Mscera  in  embryo  and  adult  (Schematic)  .4  B,  C,  position  of  organs 
in  the  embr>-o;  a,  b,  c,  position  of  organs  m  the  adult  A,  a,  normal,  B,  b,  transposition  of  the  heart  and 
arteries  simple  dextrocardia;   C,  c,  complete  situs  transversus. 


COMPLETE   AND   PARTIAL   SITUS   TRANSVERSUS. 

It  is  not  extremely  rare  to  meet  with  a  case  of  complete  transposition 
of  the  viscera,  so  that  the  heart  and  stomach  are  found  to  lie  on  the  right 
side  (dextrocardia,  dexiocardia)  and  the  liver  upon  the  left. 
This  condition  is  probably  brought  about  by  a  change  in  position  of  the 
cardiac  tube  in  early  embrj^onic  development,  so  that  it  lies  in  the  position 
of  d  instead  of  the  normal  S  (Fig.  264).  Maude  Abbott  suggests  that 
in  these  cases  there  is  a  change,  the  embryo  lies  in  an  abnormal  position 
within  the  chorion  so  that  its  right  side  instead  of  its  left  is  closer  to  the 
blood  supply.    At  all  events  the  relation  of  the  organs  is  the  mirror  image 


CONGENITAL   HEART   DISEASE. 


457 


of  the  normal  condition.  In  complete  transposition,  however,  the  organs 
develop  normally,  and  the  condition,  though  unusual,  has  no  effect  upon 
the  function.  Persons  whose  hearts  lie  on  the  right  side  are  quite  as  free 
from  symptoms  as  those  whose  hearts  are  on  the  left,  provided  the  other 
viscera  are  normal;  and  the  condition  is  usually  discovered  accidentally 
during  routine  physical  examination.    In  such  cases  the  apex  impulse  and 


PULMONARY  ARTERY 


TRICUSPID  VALVE 


AORTA 

MITRAL  VALVE 
INTERVENTRICULAR  SEPTUM 

FORAMEN  OVALE 


Fic!.  265.— Transposition  of  the  valves.  (From  a  specimen  in  the  Army  Medical  Museum,  Wash- 
ington, D.  C.)  The  course  of  the  interventricular  septum  is  indicated  upon  the  heart  wall.  The  course 
of  the  blood  stream  is  shown  by  the  arrows. 


heart  sounds  are  heard  in  the  fifth  right  interspace,  and  the  second  aortic 
is  heard  on  the  left  side  instead  of  on  the  right.  In  persons  with  thick  or 
barrel-shaped  chests,  and  especially  in  women  whose  breasts  are  large,  the 
condition  is  readily  overlooked. 

Dextrocardia  (dexiocardia)  without  transposition  of  other  viscera  is 
much  rarer.  Most  frequently  it  is  due  to  a  pushing  or  pulling  of  the  heart 
to  the  right  by  intrathoracic  growths  or  adhesions,  but  occasionally  (in  2 


PULMONARY  ARTERY 


AORTA 


Fig.  266. — Pulmonary   artery   with    four   cusps.      (From    a    specimen    in    the    Army    Meflical    Museum, 

Washington,  D.  C.) 

of  Abbott's  412  cases)  it  is  due  to  alteration  in  development.  Under  these 
circumstances  the  pulmonary  artery  is  given  off  from  the  left  ventricle, 
the  aorta  from  the  right.  Great  variations  may  be  seen  in  the  arrangement 
of  venae  cavse,  which  sometimes  enter  the  left,  sometimes  the  right  auricle. 
The  results,  as  in  other  cases  in  which  the  blood  is  mixed,  vary  greatly. 
The  syndrome  of  congenital  heart  disease  may  be  present,  owing  to  the 
mixing  of  blood,  but  the  exact  transposition  of  vessels  can  rarely  be 
diagnosed  intra  vitam. 


45S  DISEASES   OF   THE   HEART   AND    AORTA. 

ABNORMALITY   OF   THE  VALVES. 

The  number  and  formation  of  the  cardiac  valves  may  also  undergo 
alteration  in  fetal  life.  In  the  aortic  and  pulmonic  this  is  usually  due  to 
inflammatory  fusion  of  two  cusps  forming  a  bicuspid  valve  (Fig.  265), 
or  to  the  fact  that  one  of  the  leaflets  is  divided  into  two  parts  by  a  slit  and 
finally  under  the  influence  of  the  blood-pressure  grows  to  form  symmetrical 
cusps  (Fig.  266). 

In  the  mitral  and  tricuspid  valves,  especially  in  association  with  open 
septum  ventriculorum,  there  may  be  a  split  in  the  middle  of  one  leaflet, 
practically  converting  it  into  two  separate  cusps.  Except  for  the  forma- 
tion of  valvidar  insufficiencies  which  result,  multiplicity  or  paucity  of  the 
cusps  has  no  pathological  effects. 

A  large  number  of  other  malformations,  such  as  partial  separation  of 
the  two  ventricles  to  form  a  '^  bifid  apex,"  defective  formation  of  the  chest 
wall  with  exposure  of  the  heart  (ectopia  cordis),  malposition  of  the  heart 
causing  it  to  Ue  in  the  abdomen  or  the  neck,  transposition  and  malformation 
of  the  great  arteries  and  veins,  are  encountered.  Space  does  not  permit 
of  a  complete  discussion  of  these  conditions,  for  which  the  reader  is  referred 
to  the  magnificent  article  by  Dr.  Maude  Abbott  in  Volume  IV  of  Osier's 
Modern  Medicine. 

BIBLIOGRAPHY. 

Development  of  the  Normal  Heart. 

The  development  of  the  normal  heart  is  well  discussed  in  Piersol's,  Morris's,  and 
Quain's  anatomies  and  in  the  various  text-books  of  embryology. 

The  following  articles  may  be  consulted  also: 
Eternod:    Premiers  stades  de  la  circulacion  sanguine  dans  I'ouef  et  I'embryon  humains, 

Anat.  Anzeig,  1899,  xv,  181. 
His,  W.:    Anatomic  menschlicher  Embryonen,  Leipzig,  1880.     For  an  excellent  series  of 

figures  see  also  Kollman,  J.:    Handatlas  der  Entwicklungsgeschichte  des  Menschen, 

Jena,  1907. 
Born,  G.:    Beitrage  zur  Entwicklungsgeschichte  des  Saugethierherzens,  Arch.  f.  mik.  Anat., 

Bonn,  1889,  xxxiii,  p.  284. 
Robinson,  A.:    Early  Stages  of  Development  of  the  Pericardium,  J.  Anat.  and  Physiol., 

Lond.,  1903,  xxxvii,  1. 
Pohlman,  A.  G.:    The  Course  of  the  Blood  through  the  Heart  of  the  Fetal  Mammal,  etc., 

Anat.  Rec,  Phila.,  1909,  iii,  75. 

Congenital  Heart  Diseases. 

Lancereaux:  Das  anomalies  cardiaques,  Gaz.  d.  hop.,  Paris,  1880,  liii,  850,  875,  883,  890, 

906,  930,  981. 
Morgagni:  De  sedibus  et  causes  morborum,  Venet.,  1761. 
Peacock,  T.  B.:  Malformations  of  the  Human  Heart,  Lond.,  1866. 
Keith,  A.:  Malformations  of  the  Bulbus  Cordis,  Studies  in  Pathol.,  Quatercent.   Pub. 

Aberdeen  Univ.,  1906,  55. 
Bouillaud:  Traits  clinique  des  maladies  du  coeur,  Paris,  1835. 
Rauchfuss:    Missbildungen  des   Herzen's,   Gerhardt's    Handb.  d.    Kinderkrankh.,    1878, 

iv,  1  part. 
A^ierordt,  H.:  Die  angeborene  Herzkrankheiten,  Nothnagel's  Handb.  d.  spez.  Pathol,  u. 

Therap.,  Wien,  1901,  xv,  II  part  1. 
Abbott,  M.  E.:  Congenital  Cardiac  Disease,  Mod.  Med.,  ed.  by  Wm.  Osier  and  Thos.  Mc- 

Crae,  Phila.,  1908,  iv,  323. 


CONGENITAL   HEART    DISEASE.  459 

Osier,  Wm.     Quoted  from  Abbott. 

Panum,  P.  L.:  Ueber  die  Entstehung  von  Missbildungen,  Berl.,  1860. 

His,  Wm.,  Sr.:  Anatomie  menschlicher  Embryonen,  Leipz.,  1880. 

Rathke,  H.:  l^ie  Entwickelung  der  Arterien,  welche  beim  Saugethier  von  den  Bogen  der 

Aorta  ausgehen,  Arch.  f.  Anat.,  Physiol,  u.  wissench.  Med.,  Berl.,  1843,  276. 
Bremer,  J.  L.:  On  the  Origin  of  the  Pulmonary  Arteries  in  Mammals,  Am.  J.  Anat.,  Baltc, 

1901-1902,  i,  137. 
Greil,  A.:  Beitrag  zur  vergleichende  Anatomie  und  Entwickelungsgeschichte  des  Herzens 

und  des  Truncus  arteriosus  der  Wirbeltiere,  Morph.  Jahrb.,  Leipz.,  1903,  xxxi,  123. 
Hunter,  Wm.:  Medical  Observations  and  Enquiries,  1784,  vi,  300.    (Quoted  from  Peacock.) 
Kussmaul,  A.     Quoted  from  Vierordt. 
Loeb,  J.:  Ueber  die  Entwicklung  von  Fisch-embryonen  ohne  Kreislauf,  Arch.  f.  d.  ges. 

Physiol.,  Bonn,  1893,  liv,  528. 
Knower,  H.  McE.:  Effects  of  Early  Removal  of  the  Heart  and  Arrest  of  the  Circulation 

on  the  Development  of  Frog  Embryos,  Anat.  Rec.  (Am.  J.  Anat.),  Balto.,  1907. 
Mall,  F.  P.:  A  Study  of  the  Causes  underlying  the  Origin  of  Human  Monsters,  J.  Morphol., 

Phila.,  1908,  xix,  3. 
Dareste:  Recherches  sur  les  monstrosites,  Paris,  1891.     Quoted  from  Mall. 
Stockard,  C.  R.:  The  Development  of  the  Fundulus  Heteroclitus  in  Solution  of  Lithium 

Chloride,  with  Appendix  on  its  Development  in  Fresh  Water,  J.  Exper.  Zool.,  Balto., 

1906,  iii,  99. 
Bardeen,  C.  R. :  Abnormal  Development  of  Toad  Ova  fertilized  by  Spermatozoa  exposed 

to  the  Rontgen  Rays,  ibid.,  1907,  iv,  1. 
iSenac,  quoted  from  Bard,  L.,  and  Curtillet,  J.:  Contribution  a  I'^tude  de  la  physiologic 

pathologique  de  la  maladie  blue.     Forme  tardier  de  cette  affection.     Rev.  de  med., 

Paris,  1889,  ix,  993,  from  whom  Grancher  et  al.  are  quoted. 
Stille,  Moreton:  On  Cyanosis  or  Morbus  Coeruleus,  Am.  J.  M.  Sci.,  Phila.,  1844,  N.  S.  viii,  25. 
Osier,  Wm.:  Chronic  Cyanosis,  with  Polycythaemia  and  Enlarged  Spleen:  a  new  Clinical 

Entity,  Am.  J.  Med.  fe'ci.,  1903. 
Knapp,  quoted  from  Posey,  W.  C:  Cyanosis  Retinae,  Am.  J.  Med.  Sci.,  Phila.,   1905, 

cxxx,  415. 
Tate,  W.  W.  H.:  Case  of  Malformation  of  the  Heart,  Trans.  Path.  Soc,  Lond.,  1S92,  xliii,  36. 
Hebb,  R.  G.:  Hearts  with  (Congenital  Defects  and  Inflammatory  Disea.se,  ibid.,   1897, 

xlviii,  41. 
McOscar,  J.,  and  Voelcker,  A.:   On  a  Case  of   Traumatic  Rupture  of   the  Ventricular 

Septum,  ibid.,  1897,  xlviii,  47. 
Reiss,   P.:  Contribution  a  I'etude  des  malformations  congenitales  du  coeur,  Maladie  de 

Roger,  These,  Par.,  1893. 
Roger,  H.:    Recherches  cliniques  sur  la  commimication   des  cceurs   par   inocclusion   du 

septum   interventriculaire,    Bull,   de   I'Acad.   de   Med.,    Paris,    1879,   ser.  viii,    t.   ii, 

1074  and   1189. 
Cadet  de  Gassicourt,  Potain.     Quoted  from  Reiss,  1.  c. 
Klotz,  O.:  The  Closure  of  the  Ductus  Arteriosus  and  its  Bearing  on  Arteriosclerosis,  Trans. 

Asso.  Am.  Phys.,  1907,  xxii,  213. 
■Gerhardt,  C:  Persistenz  des  Ductus  arteriosus  Botalli,  Jenaische  Ztschr.  f.  Med.  u.  Natur- 

wissench.,  1867,  iii,  105.     (Quoted  from  Vierordt.) 
Zinn,  W. :  Zur  Diagnose  der  Persistenz  des  Ductus  arteriosus  Botalli,  Berl.  klin.  Wchn- 

schr.,  1898,  xx.xv,  433. 
De  la  Camp,  O. :  Familiares  Vorkommen  angeborener  Herzfehler;    zugleich  ein  Beitrag 

zur  Diagnose  der  Persistenz  des  Ductus  arteriosus  Botalli,  Berl.  klin.  Wchnschr., 

1903,  xl,  48. 
Fran^ois-Franck,  A.:  Sur  le  diagnostic  de  la  perseverance  du  canal  arteriel,  Cong,  de 

I'avancement  des  sciences,  Paris,  1878. 
-Bonnet:  Sur  la  lesion  de  la  st<?nose  de  I'isthmus  cong^nitale  de  I'aorte  dans  la  region,  Rev. 

de  M6d.,  Paris,  1903,  x.xiii,  108,  255,  335,  419,  481. 


XI. 

HEART-BLOCK  AND  THE  ADAMS-STOKES  SYNDROME. 

HISTORICAL. 

In  1827  Robert  Adams,  of  Dublin,  reported  the  case  of  a  revenue 
officer,  aged  68,  whose  pulse-rate  was  30  per  minute  and  who  suffered 
from  dyspnoea,  cough,  and  attacks  of  fainting  ("apoplectic  attacks")* 
''during  which  his  pulse  would  become  even  slower  than  usual. 
He  recovered  from  them  without  paralysis."  In  the  same  year  an  exactly 
similar  case  was  reported  in  great  detail  by  Wm.  Burnett.  Burnett's 
observations  were  reported  even  more  carefully  and  in  greater  detail  than 
those  of  Adams  and  ill  deserve  to  have  fallen  into  oblivion.  Burnett 
further  called  attention  to  the  fact  that  Morgagni  had  described  two  cases 
of  "epilepsy  with  slow  pulse"  in  1761.  Holberton  described  another  case 
in  1841,  but  general  attention  was  not  attracted  to  the  condition  until 
Wm.  Stokes  published  four  cases  in  1846. 

Since  then  the  condition  of  persistent  extreme  brady- 
cardia with  syncopal  or  convulsive  seizures  has  been 
known  as  the  Adams-Stokes  syndrome,  though  it  may  more 
accurately  be  designated  by  the  names  of  Morgagni-Adams-Stokes,  as 
Pletnew  has  done,  or  by  that  of  Morgagni-Adams-Burnett  or  Adams-Bur- 
nett syndrome. 

As  but  little  can  be  added  to  the  clinical  descriptions  of  these  cases, 
one  of  Stokes's  histories  may  be  reported  in  some  detail: 

"Edmund  Butler,  aged  68,  stated  that  his  health  had  been  robust  until  three  years 
before  admission,  at  which  time  he  was  suddenly  seized  with  a  fainting  fit.  This  occurred 
several  times  during  the  day  and  always  left  him  without  any  unpleasant  effects.  Since 
that  time  he  has  never  been  free  from  attacks  for  any  considerable  length  of  time,  and  has 
had  at  least  fifty  such  seizures.  The  fits  are  very  uncertain  as  to  their  period  of  invasion 
and  very  irregular  as  to  their  intensity,  some  being  much  milder  and  of  shorter  duration 
than  others.  They  are  induced  by  any  circumstance  tending  to  impede  or  oppress  the 
heart's  action,  such  as  sudden  exertion,  distended  stomach,  or  constipated  bowels.  There 
is  little  warning  given  of  the  approaching  attack.  He  feels,  he  says,  a  lump  first  in  the 
stomach,  which  passes  up  through  the  right  side  of  the  neck,  where  it  seems  to  explode 
and  pass  away  with  a  noise  like  thunder  by  which  he  is  stupefied.    This  is  often  accompanied 

by  a  fluttering  sensation  about  the  heart At  first  he  found  that  spirits  were  the 

best  restorative  or  prophylactic,  but  latterly  he  has  not  used  them,  being  'afraid  to  die 
with  spirits  in  his  belly.' 

"On  admission  he  was  haggard  and  emaciated On  percussion  the  chest 

is  universally  resonant.  The  respiratory  murmur  is  louder  and  combined,  especially  pos- 
teriorly, with  large  mucous  rales.    The  impulse  of  the  heart  is  slow  and  of  a  dull  heaving 

character The  first  sound  is  accompanied  by  a  soft  bruit  de  soufflet.    The  second 

sound  is  also  imperfect We  remarked  to-day  that  on  listening  attentively  to  the 

heart's  action  we  perceived  that  there  were  occasional  semi-beats  between  the  regular  con- 
tractions,— very  weak,  unattended  with  impulse,  and  corresponding  to  a  similar  state  of  the 
pulse,  which  thus  amounts  to  about  28  in  the  minute,  the  evident  beats  being  only  28.  .  .  . 
460 


HEART-BLOCK   AND   ADAMS-STOKES   SYNDROME.        461 

"  (June.)  The  cardiac  phenomena  remain  as  before,  but  a  new  symptom  has  appeared, 
namely,  a  very  remarkable  pulsation  in  the  right  jugular  vein.  This  is  most  evident  when 
the  patient  is  lying  down.  The  number  of  reflex  pulsations  is  difficult  to  be  established, 
but  they  are  more  than  double  the  number  of  manifest  contractions.  About  every  third 
pulsation  is  very  strong  and  sudden  and  may  be  seen  at  a  distance;  the  remaining  waves 
are  much  less  distinct. 

"He  has  scarcely  had  any  of  the  cardiac  attacks  since  he  was  discharged." 


RESP. 


RADIAL 


APEX 


SECONDS 


THE   CONCEPTION   OF    HEART-BLOCK. 

Stokes  did  not  appear  to  have  any  definite  understanding  of  the  nature 
of  these  ", semi-beats"  nor  of  the  functional  disturbance  associated  with 
them.  A  similar,  more  accurate  observation  was  made  by  A.  Chauveau. 
Chauveau  in  1882  made  observations  upon  a  case  whose  usual  pulse-rate 
was  24  per  minute,  and  who  suffered  from  occasional  attacks  of  vertigo 
and  loss  of  consciousness.  Tracings  made  from  the  apex  showed  a  series 
of  large  beats  at  regular  intervals  corresponding  to  the  loud  heart  sounds 
and  to  the  radial  pulse,  and  also  a  second  series  of  very  small  notches 
occurring  at  equally  regular 
intervals  but  bearing  no  rela- 
tion whatever  to  the  beats  of 
the  ventricle.  As  in  Stokes's 
case,  these  small  pulsations 
were  accompanied  by  "  small 
sounds  which  maj''  give  the  illu- 
sion of  reduplication  of  either 
heart  sound."  The  usual  pre- 
systolic notch  due  to  the  au- 
ricular beat  was  absent,  and 
Chauveau  correctly  concluded 
that  these  small  notches  were 
due  to  the  contractions  of  the  auricles,  which  were  beating  at  a 
rate  of  66  per  minute  while  the  rate  of  the  ventricles  was  24.  Chau- 
veau investigated  the  matter  experimentally,  and  was  able  to  demon- 
strate that  in  horses  upon  stimulation  of  the  vagus  the  auricles  could  be 
observed  to  beat  more  frequently  than  the  ventricles.  He  therefore  natu- 
rally considered  the  dissociation  of  auricular  and  ventricular  rhythm  as 
due  to  over-stimulation  of  the  vagus.  This  conclusion  was  further  war- 
ranted by  the  fact  that  his  patient  had  pains  at  the  back  of  the  neck,  and 
the  chief  of  service  had  diagnosticated  a  lesion  of  the  medulla  at  the  level 
of  the  vagus  nucleus. 

While  Chauveau  was  experimenting  in  France,  experimenters  in  Germany  and  in 
England  were  unconsciously  throwing  light  upon  the  condition  from  different  stand-points. 
In  1883  Wooldridge,  under  Ludwig's  direction,  was  investigating  the  course  of  the  nerves 
in  the  cardiac  septum,  and  for  this  purpose  constricted  the  interauricular  septum  by  tight- 
ening a  fine  silk  ligature  introduced  so  as  to  embrace  only  the  septum.  He  observed: 
"the  auricles  and  ventricles  continue  to  contract,  but  no  longer  with  equal  frequency. 
Stimulation  of  the  vagus  causes  the  auricles  to  stop  beating,  the  ventricles  continue. 

"The  ligature  is  removed;  at  first  the  auricles  and  ventricles  beat  at  different  rhythms, 
then  the  uniform  (normal)  beats  of  both  chambers  return,  and  stimulation  of  the  vagus 
now  inhibits  both  auricle  and  ventricle." 

Wooldridge's  results  were  confirmed  in  1884  by  Tigerstedt,  who  cut  through  the 
septum  with  a  specially  devised  "atriotome." 


Fig.  267. — Tracing  of  the  apex  beat  in  a  case  of  Adams- 
Stokes  disease,     (.^fter  Chauveau.) 


462 


DISEASES   OF   THE    HEART    AND    AOKTA. 


These  observations  under  Ludwig's  direction  were  made  with  the 
view  only  of  cutting  the  intracardiac  nerves.  As  a  matter  of  fact,  the 
muscular  connections  were  severed  as  well,  but  the  importance  of  these 
was  disregarded. 

The  myogenic  conduction  from  auricle  to  ventricle  was,  however,  at  this 
very  period  being  demonstrated  by  Gaskell  in  Cambridge  upon  the  heart 
of  the  tortoise  and  frog,  in  which  the  auriculoventricular  function  is  repre- 
sented by  a  wide  band  of  muscle  whose  properties  differ  somewhat  from 
those  of  either  the  auricle  or  the  ventricle.  Gaskell  demonstrated  that  "if 
this  auriculoventricular  ring  were  clamped,  the  auricle  continued  to  beat 
at  unaltered  rhythm,  but  as  the  clamp  was  tightened  the  period  between 
auricular    and  ventricular    contractions  (Ag-Vg  interval,   on    conduction 


A  SEC. 


JUGULAK 


APEX 


BRACH. 


Fig.  268. — Partial  heart-block  (3  : 1  rhythm)  produced  by  pressure  upon  the  vagu.s  in  a  patient  with 
disturbed  conducti\'ity  who  was  also  subject  to  attacks  of  the  Adams-Stokes  syndrome.  (Tracing  made  by 
Dr.F.  W.Peabodyand  the  writer.)   A,  A,  A,  A,  auricular  contractions  to  which  the  ventricles  do  not  respond. 


time)  was  gradually  lengthened;  then  the  ventricle  failed  to  respond  to 
some  of  the  impulses  from  the  s  auricle,  and,  according  to  the  tightness  of 
the  clamp,  the  ventricle  could  be  made  to  ...  .  respond  to  every  second 
contraction  of  the  auricles  (partial  heart-block),  to  respond  to  every  third, 
fourth,  or  other  contraction,  or  to  remain  quiescent.  When  the  clamp 
was  closed  very  tightly  the  ventricle  remained  still  for  a  variable  time, 
then,  in  accordance  to  its  inherent  rhythmical  power,  developed  a  rhythm 
of  its  own  (rhythm  of  development),  the  rate  of  that  rhythm  when  fully 
developed  and  the  length  of  time  that  the  standstill  lasted  being  correlated 
with  the  rhythmicity  of  the  tissues."  The  condition  in  which  the  ventricular 
r  ventricle  no  longer  follows  any  of  the  impulses  from  the  auricles  is  termed 
complete  heart-block,  in  contrast  to  the  partial  heart-blocks  in  which  the 
impulse  ventricle  is  responding  to  some,  but  not  all,  of  the  impulses  arising 
in  the  auricles. 

Gaskell  showed  that  heart-block  also  set  in  when  the  bridge  of  tissue 
connecting  the  auricles  and  ventricles  was  cut  down  to  a  sufficiently  nar- 
row strip.    He  was  able  to  produce  similar  blocks  between  portions  of  the 


HEART-BLOCK   AND   ADAMS-STOKES   SYNDROME.        463 

auricle  or  ventricle  by  clamping  or  cutting,  just  as  Romanes  had  clone  for 
the  muscle  in  the  bell  of  the  medusa.  Gaskell  demonstrated  also  that  the 
block  between  auricles  and  ventricles  remained  complete  when  the  only 
connection  between  the  auricles  and  the  ventricles  was  formed  by  the 
coronary  nerve. 


THE    AURICULO(aTRIO)  VENTRICULAR    MUSCLE    I5UNDLE. 

Anatomy. — The  existence  of  muscular  connections  between  the  auricles 
and  ventricles  in  man  and  mammals  was,  however,  denied  until  1893, 
when  Stanley  Kent,  of  Oxford,  found  that  in  the  rat  and  other 
mammals  there  was  a  large  strand  of  small  fusiform  muscle  cells  with 
fusiform  nuclei  which  ran  in  the  septum  membranaceum  and  connected 
the  musculature  of  the  ventricle  with  that  of  the  auricle. 

In  the  same  year  Wm.  His,  Jr.,  described  the  presence  in  the  mouse^ 
dog,  and  man  of  a  bundle  of  muscle- 
fibres  which  "arises  from  the  posterior 
wall  of  the  right  auricle  near  the  inter- 
auricular  septum,  in  the  atrioventric- 
ular groove,  lies  upon  the  upper  edge 
of  the  muscular  interventricular  sep- 
tum, passes  forwards  and  to  the  vicin- 
ity of  the  aorta,  where  it  divides  into 
a  right  and  a  left  branch.  The  latter 
passes  down  to  the  base  of  the  anterior 
mitral  cusp." 

These  anatomical  findings  of  His 
have  been  confirmed  by  Braeunig, 
Humblet,  Retzer,  and  Tawara.  The 
latter  found  that  the  fusiform  cells 
described  by  Kent  were  really  Purkinje 
fibres,  and  that  the  muscle  bundle  of 
His  is  in  reality  continuous  with  the 
entire  network  system  of  Purkinje 
fibres  which  permeates  both  ventricles. 
Tawara  also  demonstrated  the  pres- 
ence of  nerve-fibres  within  the  His  bun- 
dle, and  Gordon  Wilson  has  recently 
demonstrated    ganglion   cells   as  well. 

In  a  later  research  Retzer  has  stated  that  this  conducting  system  is 
continuous  above  with  the  septal  portion  of  the  right  auricle  (Fig.  269),  and 
that  its  cells  are  of  the  same  histological  structure  as  those  about  the  sinus 
region.  He  believes  that  it  is  a  true  sinoventricular  bundle,  but  the  recent 
work  of  Lydia  de  Witt  seems  to  confirm  the  claims  of  Tawara.  The  idea 
that  the  cardiac  impulse  must  pass  from  sinus  to  auricle  before  reaching 
the  auriculo ventricular  bundle  is  borne  out  also  by  the  observation  of  Dr. 
G.  S.  Bond  that  in  the  frog  the  auriculoventricular  muscle  can  be  seen  to 
contract  considerably  later  than  the  auricle  but  before  the  ventricle. 

Experimental  Physiology  of  the  Auriculoventricular  Bundle.  —  The 
first  experiments  upon  the  physiology  of  heart-block  in  mammals  were 


Fig.  269. — The  right  branch  of  the  auriculo- 
ventricular bundle  in  the  dog's  lieart.  (After 
Uarkerand  Hirschfelder,  Arch.  Int.  Med.,  1909.) 


464  DISEASES   OF   THE    HEART    AND    AORTA. 

performed  by  Stanley  Kent,  the  discoverer  of  the  auriculoventricular 
bundle,  in  1893,  and  were  recorded  by  him  in  his  original  publication  in 
the  following  words:  "By  the  use  of  a  suitably  constructed  clamp  ...  I 
have  been  able  to  verify  for  the  mammal  {i.e.,  in  the  excised  heart  of  the 
rat),  almost  all  the  effects  described  by  Gaskell  as  obtained  in  the  frog." 
Kent  thus  seems  to  have  forestalled  all  the  later  experiments  upon  the  sub- 
ject, but  the  brevity  of  his  physiological  note  left  much  to  be  investigated. 
In  1895  His  repeated  the  experiments  of  Wooldridge  and  Tigerstedt,  and 
demonstrated  that  in  order  to  bring  about  dissociation  of  the  auricles  and 
ventricles  it  was  not  necessary  to  injure  the  entire  septum  but  merely  this 
auriculoventricular  muscle  bundle. 

In  1899  he  applied  his  anatomical  and  physiological  studies  to  a  case 
of  Adams-Stokes  disease,  in  which  he  confirmed  Chauveau  by  finding  inde- 
pendent action  of  the  auricles  and  ventricles,  and  designated  this  by  Gas- 
kell's  term  "heart -block."  His  also  gave  an  excellent  tracing,  taken  during 
a  syncopal  attack,  demonstrating  that  the  auricles  continued  at  their 
usual  rate  while  the  ventricles  ceased  to  beat  for  several  seconds  and  then 
resumed  their  beat  at  a  gradually  increasing  rate  (corresponding  to  Gaskell's 
"rhythm  of  development"). 

1  2  3  4        5      6 


AAAAAAAAAA^'V^'vyvAAyxxv-^-^-- 


Fig.  270. — Tracings  from  the  carotid  artery  and  jugular  vein  of  a  patient  with  Adams-Stokes 
disease,  showing  stoppage  of  the  ventricles  and  continuance  of  the  auricular  contractions  during  the 
attack.  (After  His,  Deutsches  Arch.  f.  klin.  Med.,  1899,  Ixiv.)  1,  2,  3,  4,  5,  G  represent  the  onset  of 
indei>endent  ventricular  contractions. 

The  experiments  of  Kent  and  His  and  their  predecessors  were  con- 
firmed by  Humblet,  Hering,  and  Tawara,  and  led  to  the  conclusion: 

1.  That  the  slow  pulse  of  Adams-Stokes  disease  was  due  to  dissocia- 
tion between  the  auricles  and  ventricles  (heart-block)  and  to  the  slow 
independent  rhythm  of  the  ventricles. 

2.  That  the  syncopal  attacks  (Adams-Stokes  syndrome)  were  due 
to  cessation  of  ventricular  beat  but  not  of  the  auricular  beat. 

Experimentally  they  had  produced  the  former  but  not  the  latter  in 
mammals,  while  Gaskell  had  produced  it  in  the  frog  and  tortoise.  Nor 
had  pathological  changes  in  the  auricular  ventricular  bundle  been  shown 
in  cases  dying  from  the  Adams-Stokes  syndrome.  The  missing  link  was 
supplied  by  American  scientists. 

Factors  Affecting  Degree  of  Heart=block.  —  In  1904  E  r  1  a  n  g  e  r 
began  a  series  of  experimental  and  clinical  investigations  upon  this  condi- 
tion. He  first  confirmed  all  of  His's  findings  in  man,  and  refuted  Ghauveau's 
claim,  that  the  heart-block  was  due  to  the  vagi,  by  showing  that  when  in 
his  cases  the  latter  were  paralyzed  with  atropine  the  heart -block  did  not 
pass  off.^  Then  he  devised  a  modification  of  Gaskell's  clamp,  an  L-shaped 
hook  of  steel  wire  whose  arm  could  be  pressed  against  a  brass  block  by 
means  of  a  bolt  and  screw. 

*  Edes  had  previously  shown  that  belladonna  had  no  effect  in  his  cases  of  Adams- 
Stokes  disease. 


HEART-BLOCK   AND   ADAMS-STOKES   SYNDROME.       465 

The  hook  was  introduced  into  the  right  wall  of  the  aorta  just  above  its  origin  (the 
pericardial  fat  having  been  dissected  off),  the  point  passed  backwards  and  downwards 
into  the  left  ventricle,  and  then  pushed  through  the  ventricular  septum  till  it  entered  the 
right  ventricle  (Fig.  271).  The  brass  block  was  then  pushed  down  over  the  long  arm  of 
the  L  and  the  nut  gradually  screwed  taut.  The  first  effect  observed  was  lengthening  of  the 
conduction  time  (A^-Va or  A-V interval);  then  alternate  ventricular  beats  disappeared  (2  :  1 
rhji;hm),  at  first  occasionally,  then  regularly.  With  further  tightening  of  the  clamp  a 
3  :  1  rhythm  occurred,  and  finally  complete  heart-block. 
"After  the  ventricles  have  emptied  themselves  it  may  be 
seen  that  each  contraction  of  the  auricles  sends  into  the 
former  a  distinct  wave,  upon  the  subsidence  of  which  the 
volume  of  the  ventricles  is  seen  to  have  been  considerably 
increased."  In  many  but  not  in  all  of  his  experiments  the 
complete  block  began  with  a  complete  stoppage  of  the 
ventricles,  exactly  like  that  in  the  Adams-Stokes  syndrome, 
in  which  "the  ventricles  stop  beating  without  warning. 
The  auricles  continue  to  beat  with  an  apparently  unaltered 

rate The  ventricles  enlarge  with  each  contraction 

until  their  distention  becomes  really  huge Respi- 
ratory convulsions  may  begin.  Witnesses  are  almost  con- 
vinced that  the  experiment  has  come  to  a  close  when  it 
may  be  that  after  more  than  twenty  seconds  the  ventricles 
suddenly  empty  themselves  with  one  great  effort."  This  is 
sooner  or  later  followed  by  another  and  another  until  the 
slow  ventricular  rate  is  graduallv  assumed. 


Fig.  271.  — The  Erlanger 
lieart-block  clamp  compressing 
the  auriculoventricular  bundle 
(.4  V  B).  S  M,  septum  mem- 
branaceum;  MF,  mitral  valve. 


Factors  Affecting  Stoppage  of  the  Ventricles. 

—  This     ''stoppage"     of    the    ventricles 
represents  the   condition  which    is    the   cause   of 

death  and  discomfort  in  man.  Patients,  as  a  rule,  remain  free  from  symp- 
toms while  the  pulse-rate  remains  regular.  A  study  of  the  factors  bringing 
it  about  was  therefore  of  the  utmost  importance.  Erlanger  was  able  to 
show  that  it  was  neither  brought  on  nor  prevented  by  stimulation  of  the 
cardiac  nerves  when  the  heart  was  in  a  condition  of  either  partial  or  com- 
plete heart-block;  indeed  the  cardiac  nerves  exert  less  effect  than  upon  the 

vl^nlv^^AmAi>Y^\^\^^rlr- 


■  iiiiniiiiiitnii......m 


1 : 1    Clamping 


iilj  iiiiiiiiiiiiii 


Stoppage 


Undamped 


Fig.  272. — Effect  of  gradually  tightening  the  clamp.  (After  Erlanger  and  Hirschfelder.)  .Shows 
2  :  1  rhythm,  finally  stoppage  of  the  ventricles  with  complete  block.  After  this  the  ventricles  can  be  seen 
to  contract  at  an  independent  rhythm. 

uninjured  heart.  Erlanger  and  Hirschfelder  investigated  the  subject  still 
further,  and  found  that  stoppage  of  the  ventricles  occurred  when  the  clamp 
was  tightened  rapidly  and  a  complete  block  produced  suddenly.  It  occurred 
more  rarely  when  the  clamp  was  tightened  slowly,  and  the  heart  was 
allowed  to  pass  through  the  various  stages  of  partial  block  (2  :  1  and  3  :  1 
rhythm).  In  only  two  experiments  did  it  occur  after  the  ventricles  had 
already  taken  on  their  independent  rhythm.  Whenever  from  any  cause 
(stimulation  of  the  accelerators,  application  of  heat,  or  rhythmic  induction 
30 


466  DISEASES   OF   THE   HEART   AND    AORTA. 

shocks)  the  rate  of  the  auricles  was  increased,  the  degree  of  block  was  also 
increased,  a  normal  rhythm  (1:1)  passing  to  a  2  :  1,  a  2  :  1  rhythm  to  a 
4  :  1  or  to  complete  block.  When  this  occurred  rapidly  stoppage  of  the 
ventricles  sometimes  set  in.  Conversely,  slowing  of  the  auricles  from  any 
cause  (stimulation  of  the  vagus,  application  of  cold,  etc.)  improved  con- 
ductivity and  facilitated  the  passing  off  of  the  block. 

In  this  respect  the  experimental  heart-block  differs  greatly  from  the 
clinical,  since  in  a  number  of  cases  (Gibson,  Thayer)  it  has  been  found  that 
stimulation  of  the  vagus  increases  the  degree  of  block  while  atropine  re- 
moves a  partial  but  not  a  complete  block.  In  other  cases  (Edes,  Erlanger, 
Schmoll)  it  has  no  such  effect. 

The  duration  of  the  period  of  "  stoppage  "  (during  which  the  ventricles 
remained  quiescent)  varied  greatly,  and  was  greatest  in  those  hearts  which 
could  be  inhibited  longest  by  stimulation  of  the  vagus.  As  in  Gaskell's 
tortoise,  it  seemed  to  be  definitely  "correlated  to  the  rhythmicity"  of  the 
ventricles,  which  is  greater  in  some  hearts  and  at  some  stages  of  the  experi- 
ment than  at  others.  In  general  it  has  appeared  to  the  writer  that  the 
poorer  the  condition  of  the  ventricular  muscle  the  longer  the  period  of 
stoppage.  Slight  asphyxia,  though  it  did  not  in  itself  bring  about 
stoppage  of  the  ventricles,  seemed  to  lengthen  the  period  of  stoppage 
from  clamping. 

In  some  experiments  the  ventricle  remained  quiescent  for  so  long 
(more  than  55  seconds)  that  the  animal  would  have  died  at  once  had  not 
the  heart  been  revived  by  mechanical  stimulation. 

In  a  subsequent  paper  Erlanger  has  shown  that  the  condition  of  block 
on  clamping  or  injury  depends  upon  the  condition  of  the  cells  in  the  His 
bundle.  Each  cardiac  impulse  leaves  them  in  a  condition  of  lowered  irrita- 
bility from  which  they  recover  gradually.  When  the  injury  is  slight  they 
recover  just  too  late  for  the  next  impulse  from  the  auricle  and  are  only 
ready  to  receive  the  second  stimulus  (a  2  :  1  rhythm  resulting).  When 
they  are  injured  a  little  more  they  recover  in  time  for  every  third  or  every 
fourth  impulse,  and  finally  the  stimulus  always  remains  below  the  threshold 
of  irritability  and  complete  block  sets  in.  Similarly,  the  more  rapid  the 
rhythm  the  less  time  the  cells  have  had  to  recover  and  the  less  the  intensity 
of  impulse  from  the  auricles,  hence  the  greater  the  block. 

As  regards  the  ventricle,  the  greater  its  irritability  and  rhythmicity 
the  sooner  it  will  respond  to  its  own  internal  stimuli  with  a  contraction 
and  the  shorter  the  stoppage  and  the  more  rapid  the  rhythm.  A  low  ven- 
tricular rhythm  (under  25  per  minute)  is  therefore  often  a  sign  of  poor 
condition  of  the  ventricle  and  of  a  tendency  to  stoppage  during  the  period 
of  complete  block  in  spontaneous  attacks. 

The  experiments  of  Erlanger  and  Hirschfelder  have  been  confirmed 
by  V.  Tabora  under  Hering's  direction.  The  latter  has  found  that  stimu- 
lation of  the  vagus  may  under  certain  circumstances  increase  the. degree 
of  heart-block  and  facilitate  the  onset  of  stoppage,  especially  when  digi- 
talis has  been  administered.  The  apparent  discrepancy  between  their 
findings  is  probably  due  to  the  presence  of  the  different  nerve-fibres 
in  the  vagus,  so  that  sometimes  conductivity,  sometimes  irritability  is 
most  afTected. 


HEART-BLOCK  AND   ADAMS-STOKES   SYNDROME.       467 


RELATION    OF    HEART-BLOCK    TO    ADAMS-STOKES    SYNDROME. 

It  cannot  be  too  strongly  emphasized  that:  (1)  heart-block  (complete) 
and  Adams-Stokes  syndrome  are  by  no  means  synonymous;  the  former 
represents  merely  the  dissociation  of  rhythms,  while  the  Adams-Stokes 
syndrome  brought  on  by  cerebral  anaemia  during  ventricular  stoppage  is 
a  totally  different  matter;  (2)  heart-block  may  persist  for  months  or  years 
without  the  occurrence  of  the  syndrome,  as  in  the  case  about  to  be  described. 

Attacks  of  the  Adams-Stokes  syndrome  may  occur  in  three  ways: 
(1)  at  the  transition  from  normal  rhythm  to  complete  block;  (2)  in  the 
midst  of  complete  block;  (3)  probably  also  from  stimulation  of  the  vagus 
in  certain  cases  where  conductivity  is  already  diminished. 

In  the  cases  where  the  Adams-Stokes  syndrome  (ventricular  stoppage) 
appears  at  the  transition  from  normal  rhj^thm  to  complete  block,  the  attacks 
are  usually  preceded  by  quickening  of  the  pulse;  and  the  block  passes  off 
and  reappears  suddenly.  When  the  complete  block  becomes  permanently 
established,  the  Adams-Stokes  syndrome  may  disappear,  as  is  well  shown 
by  the  following  case,^  seen  by  the  writer  in  consultation  with  Dr.  H.  G. 
Beck.  The  Adams-Stokes  syndrome  may  be  present  only  in  the  initial 
and  not  the  later  stages  of  the  heart-block. 

Case  of  Heart-block,  with  Adams-Stokes  Syndrome  only  at  Onset  of  Block. 

J.  L.,  aged  72,  had  been  perfectly  healthy  all  his  life  except  for  attacks  of  malaria 
when  between  14  and  40  years  of  age,  and  pneumonia  about  ten  years  ago.  Denies  syphilis 
and  gonorrhcea;  drinks  little,  but  smokes  considerably.  Has  been  a  blacksmith  until 
July,  1907.  At  this  time  he  was  struck  on  the  head  by  a  railroad  gate,  became  unconscious 
for  one  or  two  minutes,  after  which  he  recovered  at  once  except  for  a  slight  transitory 
weakness  of  the  right  arm  and  slight  transitory  aphasia.  He  remained  well  until  Novem- 
ber, 1907,  pulse  being  60  to  64.  In  the  latter  part  of  November  he  began  to 
have  weak  spells  in  which  he  fell  but  did  not  lose  consciousness.  He  was  seen  by 
the  writer  on  January  12,  when  he  had  been  having  numerous  attacks  for  about  a  week. 


Fig.   273. — Tracing   from   jugular  vein  and   carotid   artery,   in   a   case   (J.   J^.)   of  complete  heart-block 
after  the  syncopal  attacks  had  subsided. 

Patient  was  a  fairly  nourished  man  of  good  rosy  color,  pupils  reacting  normally;  no  signs 
of  intracranial  disturbance  nor  of  lues.  Chest  clear.  Heart  not  enlarged;  action  regular; 
p  u  1  s  e  -  r  a  t  e  33  per  minute.  Sounds  accompanying  the  beats  are  loud  and  the  first 
sound  is  accompanied  by  a  flowing  systolic  murmur  not  transmitted  to  axilla.  Second 
sound  clear.  Between  these  in  the  long  pause  there  can  be  heard  two  or  three 
very  soft  distant  sounds  like  the  ticking  of  a  watch,  accompanying  which 
small  undulations  may  be  seen  over  the  jugular  vein,  and  on  most  delicate 
palpation   of   the    radial   a   slight   impulse   can   be   felt   there   as 

■  A  study  of  this  case  has  been  reported  by  Drs.  H.  G.  Beck  and  W.  R.  Stokes,  Arch. 
Int.  Med.,  Chicago,  190S. 


468  DISEASES   OF   THE    HEART    AND    AORTA. 

well,  due  to  the  beating  of  the  auricles  against  the  root  of  the  aorta.  The  venous 
tracing  (Fig.  273)  showed  complete  heart-block.  At  this  time  he  had  no  attacks.  On 
January  17,  however,  he  was  again  seen.  His  attacks  had  been  very  numerous,  the  pulse- 
rate  rising  and  falling  with  great  rapidity.  Tracings  from  the  jugular  vein  and  carotid 
arteries,  taken  as  an  attack  came  on,  show  the  foUowng  sequence  events:  At  first  a  period 
of  complete  heart-block  lasting  a  few  minutes.  This  then  passed  off  and  was 
succeeded  by  a  few  moments  of  2:1  r  h  y  t  h  m  .  The  2  :  1  rhythm  passed  suddenly 
into  a  1  :  1  rhythm  at  a  rate  of  about  90  per  minute  and  began  to  quicken. 
It  was  then  prophesied  that  an  attack  was  imminent,  and  in  an  instant  the  vent  ri- 
des suddenly  ceased  to  beat.  The  patient  cried  out,  became  ashy  pale,  and  a 
convulsion  set  in,  during  which  the  auricles  continued  to  beat  at  the  old  rate.  In 
about  11  seconds  the  ventricles  began  to  beat,  and  soon  resumed  their  regular  independent 


Fig.  274.  —  Diagram  representing  the  conditions  found  in  the  tracing  Fig.  273.  .4,  auricular 
contractions ;  V,  ventricular  contractions ;  1,  2,  first  and  second  heart  sounds ;  a,  a,  sounds  due  to 
contractions  of  the  auricles. 

rate  of  28  to  30  per  minute  in  comjjlete  block.  After  a  few  more  seizures  an 
hour  or  so  passed  without  further  change  in  rate  or  further  symptoms.  When  seen  in  the 
afternoon  and  again  on  the  next  day  the  pulse-rate  had  not  varied.  It  was  then  prophesied 
by  the  writer  that  no  more  attacks  were  imminent,  but  the  patient  was 
kept  in  bed  for  several  weeks  afterwards.  A  few  weeks  later  he  had  a  sinking  spell  with 
weakness  of  the  pulse,  but  no  change  in  rate  and  regularity  and  no  unconsciousness  or 
convulsions.  This  he  also  recovered  from  and  remained  free  from  symptoms  and  attacks 
imtil  his  death  two  months  later.  He  died  rather  suddenly  but  was  conscious  to  the  last; 
his  pulse-rate  had  not  changed,  and  he  died  not  from  the  Adams-Stokes  syndrome  but 
from  his  coronarj*  sclerosis.  The  lesion  found  in  the  His  bundle  will  be  discussed  below. 
In  this  patient  the  Adams-Stokes  syndrome  passed  off  as  the  com- 
plete  block  became   established. 

Variations  in  Pulse=rate. — This  case  is  no  isolated  example  of  such  a 
condition.  Even  Burnett's  case  (1824)  furnishes  an  example,  for  he  says, 
"the  pulse  beats  at  the  rate  of  74  in  the  minute  for  the  space  of  about  a 

minute,  then  intermits  for  7,  8,  or  10  seconds In  the  evening  I 

found  that  he  had  been  attacked  many  times  but  was  then  much  better. 
....  He  complained,  however,  of  more  pain  about  the  precordia  and 
his  pulse  beat  only  20  in  the  minute."  A  similar  tendency  to  improvement 
after  heart-block  set  in  has  been  noted  in.  Stokes's  first  case  (1846),  in  that 
of  Alfred  Webster  (1900),  in  one  of  the  cases  reported  by  Edes  (1901),  and 
in  one  of  Erlanger's  cases  (1905). 

Stoppage  of  the  Ventricles  during  Complete  Heart=block.  —  Unfortu- 
nately, the  Adams-Stokes  syndrome  does  not  always  end  with  the  estab- 
lishment of  permanent  complete  block.  Just  as  in  the  two  experiments 
of  Erlanger  and  Hirschfelder  mentioned  above,  stoppage  of  the  ventricles 
sometimes  occurs  in  the  midst  of  a  complete  block  when  the  pulse-rate  is 
slow  and  without  preliminary  variations  in  rate.  This  took  place  in  the 
case  reported  by  His  and  in  Erlanger's  first  case.  The  influences  producing 
this  stoppage  act  directly  upon  the  ventricles,  the  auricular  rate  being 


HEART-BLOCK   AND   ADAMS-STOKES    SYNDROME.        469 


Fig.  275. — Heart  of  a  patient  (J.  L.)  showing  calcifications  which  produced  Adams-Stokes  disease, 
(Drawn  from  the  specimen.)  A,  B,  C,  D,  E.  Sections  through  the  inter\'entricular  septum,  showing  the 
calcification  pressing  upon  the  auriculoventricular  bundle.  (After  Beck  and  Stokes.)  F.  Section  through 
a.     cPhotomicrograph  by  Dr.  C.  S.  Bond.) 


470 


DISEASES   OF   THE    HEART   AND   AORTA. 


unchanged  or  quickened,  but  the  nature  of  these  influences  is  not  well 
understood.  Erlanger  has  shown  that  the  plugging  of  a  coronary  artery 
in  animals  does  not  bring  stoppage  from  complete  block.  On  the  other 
hand,  slight  asphyxia,  such  as  holding  the  breath  after  slight  exercise, 


Fig.  276. — Diagram  showing  the  two  types  of  ventricular  stoppage  producing  the  Adams-Stokes 
sjTidrome.  1.  Ventricular  stoppage  only  at  the  moment  when  conduction  ceases.  2.  Stoppage  of  the 
ventricles  setting  in  during  the  periods  of  complete  block.  .4,  auricular  contractions;  T',  ventricular 
contractions;    A-V,  conduction  of  impulses  from  auricles  to  ventricles. 

brought  them  on  regularly.  However,  it  cannot  be  said  that  the  prognosis 
is  much  if  any  more  unfavorable  in  these  than  in  the  other  group  of  cases, 
since  Erlanger's  case  at  least  lived  several  years  after  observation,  and 
this  point  has  not  been  noted  in  most  of  the  reported  cases.  Prof.  Thayer 
has  recently  reported  a  case  in  which  the  block  has  passed  off. 


LESIONS    OF    THE    AURICULOVENTRICULAR    BUNDLE. 

These  two  groups  represent  cases  in  which  the  block  appears  to  be 
myogenic;  and  pathological  evidence  indicates  that  such  is  the  case.  Al- 
though Adams  (1827)  mentions  fatty  degeneration  of  the  ventricular  septum 

in  his  case,  and  many  other  au- 
topsies had  been  performed,  the 
first  case  in  which  a  lesion  of  the 
auriculoventricular  (or  atrioven- 
tricular) muscle  bundle  was 
demonstrated  was  that  of  Luce 
in  1902  in  which  a  sarcoma  was 
found  involving  the  auriculoven- 
tricular bundle.  Luce,  however, 
did  not  regard  this  as  a  causal 
factor  for  the  Adams-Stokes  syn- 
drome, and  the  first  case  in  which 
this  connection  was  definitely 
established  was  reported  by  Sten- 
gel, of  Philadelphia,  in  1905,  with 
excellent  figures  showing  fibrosis 
of  the  bundle.  Soon  after  this 
Schmoll  reported  a  case  in  which 
no  lesion  could  be  discovered 
macroscopically,  but  fibrosis  of 
the  His  bundle  was  demonstrated  with  the  microscope. 

In  the  case  of  J.  L.  reported  above,  autopsy  showed  extensive  atheroma 
of  the  aorta;  the  coronary  arteries  were  converted  into  pipes  of  bony  hard- 


FiG.  277. — Section  of  a  luetic  infiltration  of  the 
auriculoventricular  bundle.  (After  Ashton  N  orris  and 
Lavenson.)     INF.,  area  of  round-cell  infiltration. 


HEART-BLOCK  AND   ADAMS-STOKES   SYNDROME.       471 

iiess.  Large  calcifications  were  present  upon  the  mitral  valve  and  in  the 
upper  part  of  the  interventricular  septum,  in  which  a  long  tongue  of  calci- 
fication can  be  seen  to  intercept  the  auriculoventricular  bundle.  This  was 
beautifully  shown  in  the  sections  which  were  made  by  Stokes  under  Retzer's 
direction,  and  thoroughly  explain  the  clinical  features  observed. 

In  the  past  two  years  a  considerable  number  of  cases  have  been  studied 
both  histologically  and  physiologically,  lesions  in  the  His  bundle  being 
uniformly  found.    The  following  represent  some  of  the  lesions  reported: 

Gumma,  7:'Handford  (1904),  Keith  and  Miller  (1906),'Grunbaum  (1906),-Ashton, 
JS'orris,  and  Lavenson  (1907),  Heineke  (1907^'Fahr  (1907),'Rendu  (1895). 

Calcified  patches  involving  the  bundle,  4 r  Stengel  (1905), 'Hay  and  Moore  (1906), 
•JBeck  and  Stokes  (1908), 'Heineke,  Muller,  and  Hoesslin  (1908). 

Fibrosis  of  the  bundle,  6:-Schmoll  (1906),. Gibson,  G.  A.  (1906),  Fahr  (1907),-Gib8on, 
A.  G.  (1908),  Dock,  G.,»Vaquez  and  Esmein. 

Tumors  in  the  septum:  Fibroma >Sendler   (1892).     Round-celled  sarcoma: » Luce. 

Anaemic  infarction  of  the  auriclo(atrio) ventricular  bundle:  'Jellinek,  Cooper,  Ophiils 
(1906),  MacCallum  (1908).  -^ 

Simple  round-celled  infiltration  of  the  auriculoventricular  bundle,  1:  '  Heineke, 
Muller,  and  Hoesslin  (1908). 

Mural  ulceration  involving  the  auriculoventricular  bundle  (ulcerative  endocarditis) : 
James  (1908). 

Fatty  degeneration:  > Butler  (1907). 

Arteriosclerosis  of  artery  supplying  auriculoventricular  bundle:  -D.  Gerhardt  (1908). 

Absence  of  demonstrable  lesion,  macroscopic  or  microscopic:  Heineke,  Muller,  and 
Hoesslin  (1908). 

CASES    OF    ADAMS-STOKES    SYNDROME    NOT    DUE    TO    LESION    OF    THE 
AURICULOVENTRICULAR    BUNDLE. 

Although  the  overwhelming  majority  of  cases  of  the  Adams-Stokes 
syndrome  (persistent  bradycardia,  complete  heart-block,  and  syncopal 
attacks)  have  been  proved  to  be  due  to  lesions  of  the  auriculoventricular 
"bundle,  a  few  cases  in  the  literature  remain  which  must  still  be  regarded 
as  due  to  over-stimulation  of  the  vagus. 

The  most  typical  of  these  attacks  is  described  by  Thanhoffer  (1875).    A  colleague  was 

'  compressing  his  own  vagi  in  the  neck,  when  suddenly  he  "  stared  at  me  with  glassy  eyes, 

without  releasing  his  grip  and  without  answering.    I  could  remove  his  hand  from  his  throat 

only  with  the  greatest  force  and  they  still  remained  clenched.     Consciousness  did  not 

immediately  return  even  after  removing  his  hands." 

Another  case  was  reported  by  Neuberger  and  Edinger  in  1898:  The  patient  was  a 
neurasthenic  man,  aged  46,  who  had  been  repeatedly  examined  by  various  physicians  but 
no  signs  of  organic  nervous  disease  discovered.  He  suffered  from  severe  constipation. 
From  Nov.,  1896,  to  January,  1897,  he  occasionally  fainted  when  at  stool.  His  pulse  dur- 
ing that  period  was  usually  60  between  attacks.  On  January  1,  1897,  he  fell  in  a  faint  while 
having  a  desire  to  go  to  stool ;  his  head  and  eyes  were  drawn  to  the  left  and  the  eyes  twitched. 
During  that  day  he  had  several  similar  attacks,  before  each  of  which  the  pulse  disappeared, 
returning  during  the  attack  to  a  rate  of  16  to  18  per  minute.  By  evening  the  rate  had 
returned  to  60.  He  died  in  one  of  these  attacks  on  January  8.  Autopsy,  performed  by 
Carl  Weigert,  showed  almost  complete  atrophy  of  the  right  half  of  the  cerebellum  and  a 
varicose  dilatation  of  the  ependymal  vessels  in  the  medulla.  It  is  probable  that  at  stool 
or  during  effort  the  pressure  in  these  varices  rose  and  caused  them  to  compress  the  medulla 
near  the  vagus  nucleus.  In  spite  of  a  very  careful  search  by  Weigert,  no  myocardial  lesion 
could  be  found.  It  is,  therefore,  fair  to  assume  that  in  this  case  the  attacks  and  the  prob- 
ably existing  heart -block  were  vagal  in  origin. 

Dr.  Walter  James  also  reported  a  case  in  which  recurrent  groups  of  ineffectual  extra- 
systoles  caused  the  circulation  to  become  so  slow  at  times  as  to  produce  syncopal  attacks. 


472  DISEASES   OF   THE   HEART    AND    AORTA. 

A  somewhat  similar  case  was  that  of  Holberton  (1.  c.)  (1841),  in  which  the  attacks 
dated  from  a  fall  from  a  horse,  and  no  myocardial  lesion  was  found.  On  the  other  hand, 
our  case  (page  467)  illustrates  the  need  of  caution  in  reaching  this  conclusion,  since  there 
the  attacks  dated  from  a  blow  upon  the  head,  and  yet  autopsy  proved  the  presence  of  a 
most  typical  lesion  of  the  auriculoventricular  bundle.  Since  these  lesions  may  be  micro- 
scopic (Schmoll,  Gerhardt),  it  is  evident  that  a  neurogenic  origin  of  the  syndrome  can  be 
^diagnosed  only  when  the  bundle  has  been  examined  by  serial  sections.  The  writer  has 
also  seen  in  consultation  a  case  of  complete  heart-block  associated  with  a  timior  along  the 
course  of  the  vagus. 

Since  it  requires  a  very  considerable  lesion  to  produce  the  neurogenic 
syndrome,  and  since  death  occurs  from  the  latter  cause  as  well  as  from 
the  syndrome,  the  prognosis  is  no  better  in  these  cases  than  in  the  myogenic, 
except  in  cases  where  the  causal  factor  (tumor,  etc.)  may  be  removed  by 
operation  or  by  treatment.  However,  it  must  be  added  that  even  with 
the  most  liberal  interpretation  neurogenic  cases  are  extremely  rare,  and 
the  presence  of  the  Adams-Stokes  syndrome  may  almost  always  be  regarded 
as  prima  facie  evidence  of  a  lesion  of  the  auriculoventricular  bundle. 

Atropine  Test. — The  origin  of  the  block  in  these  cases  can  be  readily 
demonstrated  by  paralyzing  the  vagi  by  the  administration  of  atropine, 
1  mg.  (^V  gr.),  which  causes  the  block  to  pass  off  in  the  neurogenic  cases 
and  the  pulse-rate  to  become  rapid,  but  does  not  affect  it  in  the  myogenic. 
In  most  cases  of  the  typical  Adams-Stokes  disease  (Edes,  Erlanger,  Schmoll), 
atropine  does  not  affect  the  rate,  and  the  organic  nature  is  further  proved. 
In  our  own  two  rather  exceptional  cases  the  atropine  test  was,  unfortunately, 
not  permitted.  Gibson  and  Ritchie  have  reported  a  most  interesting  case 
in  which  both  neurogenic  and  myogenic  factors  seemed  to  be  at  work,  since 
the  complete  block  disappeared  promptly  upon  giving  atropine  and  reap- 
peared an  hour  later  when  the  effect  had  worn  off.  However,  conductivity 
was  always  diminished  (conduction  time,  a-c  interval,  being  0.6  second 
instead  of  0.2)  even  when  the  vagi  were  paralyzed,  so  that  the  auriculo- 
(atrio) ventricular  bundle  was  probably  injured  as  well.  Professor  Thayer 
and  Dr.  F.  W.  Peabody  have  found  that  atropine  caused  the  partial  block 
(4  :  1  rhythm)  to  pass  off,  but  had  no  effect  when  the  block  was  complete. 
This  observation  harmonizes  well  with  the  other  experimental  and  cUnical 
evidence  regarding  complete  and  partial  blocks. 

CONTRIBUTING    FACTORS. 

The  Adams-Stokes  syndrome  is  more  common  in  men  (84  per  cent, 
of  Edes's  cases),  of  which  48  per  cent,  occurred  between  the  ages  of  50 
and  70.  This,  as  well  as  the  autopsy  series  mentioned  above,  establishes 
the  importance  of  coronary  sclerosis  as  an  etiological  factor.  It  is  quite 
striking  that  in  two  cases  of  this  small  series  (that  of  Cooper,  Jellinek,  and 
Ophiils  and  one  of  those  mentioned  by  Dietrich  Gerhardt)  gonorrhoeal 
infection  was  the  etiological  factor.  Mackenzie  describes  cases  of  partial 
heart-block  (2  :  1  rhythm)  as  a  result  of  influenza  and  pneumonia,  and  the 
writer  has  seen  a  similar  depression  of  conductivity  during  the  course  of 
the  latter.  Powers  has  reported  a  case  with  partial  halving  of  the  rate 
after  pneumonia.  Saigo  has  found  extensive  vacuolization,  fatty  and  paren- 
chymatous degeneration,  and  cellular  infiltration  in  the  Purkinje  fibres 
of  the  conduction  system  following  acute  rheumatism  and  other  diseases. 


HEART-BLOCK   AND   ADAMS-STOKES   SYNDROME.        473 

These  were  especially  marked  in  the  left  branch  of  the  auriculoventricular 
bundle.  The  importance  of  infectious  diseases  as  directly  causal  factors 
is  further  shown  by  the  case  of  Butler,  in  which  the  bradycardia  dated 
from  an  attack  of  typhoid  fever,  and  also  in  Dunn's  case,  in  which  a  radial 
pulse  (18  per  minute)  and  typical  Adams-Stokes  syndrome  occurred  in  a 
boy  of  1 1  on  the  ninth  day  of  diphtheria.  There  can  be  no  doubt  that  many 
of  the  sudden  deaths  from  pneumonia  and  diphtheria  are  due  to  heart-block. 

Cardiac  overstrain  may  also  be  a  factor,  as  in  the  case  of  a  boy  of  15 
reported  by  Striibing,  who  when  otherwise  healthy  ran  a  considerable 
distance,  fainted,  then  walked  home,  and  had  several  other  syncopal  attacks 
with  convulsions.  His  heart  was  enlarged,  and  the  pulse  16  to  18  per  minute. 
Rest  and  proper  treatment  brought  about  some  improvement,  and  his 
pulse  finally  rose  to  44,  but  he  died  soon  afterwards. 

It  is  possible  that  ptomaine  poisoning  or  autointoxication  due  to  severe 
gastro-intestinal  upset  may  give  rise  to  the  syndrome. 

Case  op    Adams-Stokes  Disease  with  Subsidence  and  Recurrence  of    Symptoms, 
AND  WITH  Attacks  during  Complete  Block. 

Recently  the  writer,  with  Professor  Thayer  and  Dr.  H.  M.  Thomas,  examined  a  gentle- 
man who  had  lately  suffered  from  a  severe  acute  gastro-enteritis  with  vomit- 
ing and  severe  diarrhcBa  lasting  several  days.  During  this  time  he  had  fainted  several 
times  while  at  stool,  and  his  physician  found  him  with  a  pulse-rate  of  20  per 
minute.  With  the  improvement  in  digestion  this  bradycardia  passed  off  within  a  few  days, 
and  he  had  no  further  syncopal  attacks.  When  examined  ten  days  later  his  pulse- rate  was 
60,  increasing  normally  upon  slight  exercise.  There  was  no  sign  of  heart-block,  and  con- 
duction time  {a-c  interval)  was  normal  (0.2  second).  No  signs  of  nervous  disturbance 
were  present.  After  a  few  weeks  of  good  health  the  fainting  spells  and  bradycardia  returned, 
and  lasted  for  several  months.  Prof.  Thayer  informs  the  writer  that  during  this  period 
the  rhythm  varied  from  1:1  to  2:1  and  4:1,  returning  to  normal 
rate  when  atropine  was  administered.  Syncopal  attacks  also 
occurred  frequently  in  the  midst  of  complete  heart-block,  and 
during  the  periods  of  complete  heart-block  the  rate  was  very  slow  and  irregular.  In 
complete  block  the  rate  was  unaffected  by  atropine. 

After  some  months  conductivity  gradually  returned,  and  at  the  time  of  writing  the 
patient  has  remained  quite  well  and  has  had  a  normal  pulse- 
rate   for   several   months. 

The  presence  of  a  hemorrhage  in  the  auriculoventricular 
bundle  or  its  vicinity  (apoplexy  of  the  bundle)  would  account 
for  the  occurrence  and  the  subsidence  of  these  symptoms.  An 
infiltration  or  fatty  degeneration  of  the  bundle  might  account  for  the  occurrence  and 
subsidence  of  the  first  attack,  but  scarcely  for  the  sudden  recurrence  during  a  period  in 
which  the  patient  had  been  in  excellent  health. 

Prentiss  also  mentions  a  case  brought  on  by  heavy  lifting,  in  which 
either  hemorrhage  or  myocardial  degeneration  may  have  been  the  cause. 

Partial  heart-block  has  been  reported  from  over- 
doses of  digitalis  (Mackenzie,  Hewlett,  A.  G.  Gibson)  (page  179), 
but  these  have  never  given  rise  to  complete  block  or  Adams-Stokes 
syndrome. 

PHYSICAL    SIGNS    AND    DIAGNOSIS. 

As  the  Adams-Stokes  syndrome  may  occur  in  cases  having  valvular 
lesions,  the  physical  signs  over  the  heart  may  vary,  and  all  forms  of  mur- 
murs and  of  cardiac  insufficiency  may  occur.    Those  which  are  character- 


474  DISEASES   OF   THE   HEART   AND    AORTA. 

istic  of  the  condition,  as  observed  by  Stokes  and  Chauveau,  are  the  very 
slow  pulse  disappearing  entirely  before  the  onset  of  the  attack;  the  presence 
of  small  visible  pulsations  in  the  jugulars,  of  more  than  double  the  number 
of  the  pulse  in  the  carotids,  with  the  small  jugular  pulsations  and  occurring 
at  a  regular  rhythm  which  is  more  rapid  than  that  of  the  ventricles;  a  faint 
sound  like  the  ticking  of  a  watch  may  often  be  heard  near  the  left  sternal 
margin,  i.e.,  the  right  auricle;  and  a  slight  pulsation  or  shock  may  at  the 
same  time  be  seen  or  felt  over  the  apex.  On  most  careful  palpation  a  faint 
shock  of  the  same  rhythm  may  also  be  felt  in  the  radial  pulse.  This  corre- 
sponds to  the  small  auricular  wavelets  upon  the  pulse,  which,  as  Frangois- 
Franck  has  shown,  are  due  to  the  beating  of  the  auricles  against  the  root 
of  the  aorta. 

All  these  signs  may  usually  be  made  out  in  cases  of  heart-block,  and 
the  diagnosis  should  therefore  be  made  by  any  clinician  in  the  ordinary 
physical  examination. 

In  X-ray  examination  the  independent  contraction  of  the  auricles 
may  be  readily  seen  (Deneke),  and  this  of  course  settles  the  diagnosis.  Sim- 
ilarly G.  A.  Gibson  and  Einthoven,  as  well  as  Barker,  Bond,  and  the  writer, 
have  demonstrated  heart  block  by  the  electrocardiogram. 

The  usual  and  the  most  satisfactory  method  of  diagnosis  is  by  com- 
parison of  the  venous  pulse  tracing  with  that  from  the  carotid  artery  or 
the  apex,  by  which  means  the  exact  relation  of  auricular  to  ventricular 
contraction,  the  degree  of  block,  and  the  variations  of  conductivity  are 
readily  shown. 

Diflficulties  in  diagnosis  may  occur  from  the  following  causes: 

1.  The  pulse-rate  may  be  so  slow  that  heart-block  may  be  suspected. 
This  occurs  especially  in  old  persons,  in  athletes  when  at  rest,  and  in  con- 
valescents from  infectious  diseases.  For  the  absolute  exclusion  of  heart- 
block  a  venous  tracing  may  be  necessary,  in  which  the  absence  of  a  wave 
midway  between  the  normal  a  waves  excludes  the  presence  of  a  heart- 
block.  The  writer  has  seen  a  number  of  cases  whose  pulse-rate  was  44  to 
48  per  minute  with  no  sign  of  heart-block  on  the  venous  tracing.  (Figs. 
48  and  106.) 

2.  The  early  diastolic  wave  (h  wave  of  Hirschfelder,  b  wave  of  Gibson) 
may  sometimes  occur  midway  between  auricular  waves,  and  may  thus 
simulate  a  2:  1  rhythm.  Moreover,  the  "third  heart  sound"  is  usually 
present  in  these  cases,  and  may  easily  be  taken  for  the  sound  of  auricular 
contraction.  The  presence  of  the  h  wave  may  be  differentiated  from  that 
of  partial  block  by  increasing  the  heart-rate,  by  rapid  respiration,  mild 
exercise,  etc.,  upon  which  the  h  wave  is  no  longer  found  midway  between 
a  waves,  but  maintains  its  old  interval  from  the  v  wave  and  approaches 
the  second  a,  whereas  in  partial  heart-block  it  would  maintain  the  mid- 
position.  This  point  is  of  great  importance,  since  the  presence  of  heart- 
block  is  a  grave  sign,  and  it  should  not  be  diagnosed  without  due  care. 
The  writer  has  seen  a  number  of  cases  in  which  heart-block  might  have 
been  diagnosed  had  this  precaution  not  been  exercised,  as  for  example  the 
patient  whose  phlebogram  is  shown  in  Fig.  106. 

Slow  pulse  of  vagal  origin  may  also  occur  in  brain  tumor, 
fracture  of  the  skull,  meningitis,  etc.,  and,  especially  in  the  first,  may  be 


HEART-BLOCK  AND   ADAMS-STOKES   SYNDROME.       475 

accompanied  by  syncopal  attacks.  In  these  cases  there  is  rarely  any  degree 
of  heart-block  between  attacks,  and  the  site  of  the  cardiac  disturbance 
can  readily  be  determined  by  its  disappearance  after  the  administration 
of  atropine. 

A  slow  pulse  with  occasional  attacks  of  vertigo  may  also  occur  as  the 
result  of  extrasystoles  too  weak  to  open  the  aortic  valves,  and  thus 
give  rise  to  a  rhythm  which  is  too  slow  to  nourish  the  brain  (W.  James), 
and  a  true  Adams-Stokes  syndrome  arises  without  heart-block.  The  diag- 
nosis is,  however,  readily  made  on  ausculation,  from  the  fact  that  between 

effective  beats  a  single  loud  sound  is  heard  (whole  rhythm  being  lub  dub 

1  12  1 

lub,  pause, lub  dub  lub)  and  not  the  feeble  ticking  auricular  sound 

of  auricular  contractions.  The  venous  pulse  and  electrocardiogram  char- 
acteristic of  extrasystoles  (see  page  68)  establish  the  diagnosis. 

In  occasional  cases,  paroxysms  of  tachycardia  are  accom- 
panied by  fainting  spells,  the  pulse  between  attacks  being  quite  normal 
or  even  very  slow. 

Case  of  Paroxysmal  Tachycardia  with  Syncopal  Attacks,  Suggesting 
Adams-Stok^s  Disease. 

A  few  years  ago  the  writer  examined  such  a  case  in  consultation  with  Professor  Barker 
and  Dr.  I.  P.  Lyon  of  Buffalo.  The  patient  was  a  man  past  middle  age,  had  a  pulse-rate 
of  60,  and  had  been  subject  to  attacks  of  palpitation  with  fainting  spells.  The  case  had 
been  seen  by  several  specialists  in  various  cities,  who  had  diagnosed  it  Adams-Stokes 
syndrome.  Physical  examination  was  negative  except  for  a  slight  grade  of  arteriosclerosis. 
Tracings  of  the  venous  pulse,  however,  showed  conductivity  to  be  normal  {a-c  interval 
0.2  second),  and  this  continued  to  be  the  case  even  when,  upon  exercise,  the  pulse-rate 
rose  to  120  per  minute  without  dropping  a  beat.  The  Adams-Stokes  syndrome  was  thus 
excluded.  From  the  sudden  onset  and  the  fainting  spells  during  the  attacks,  it  was  con- 
cluded that  the  condition  was  most  probably  paroxysmal  tachycardia.  The  patient  was 
subsequently  seen  in  a  typical  attack,  with  sudden  approximate  doubling  and  sudden 
halving  of  the  rate,  and  the  diagnosis  was  thus  verified.  Dr.  Lyon  informs  the  writer  that 
the  patient  is  much  improved  and  has  now  only  mild  attacks  of  tachycardia. 

There  may  occasionally  be  difficulty  in  differentiating  the  Adams- 
Stokes  syndrome  from  epilepsy  and  brain  tumor.  Heart-block  is,  however, 
never  present  in  the  former,  very  rarely  in  the  latter;  so  that  the  diagnosis 
can  usually  be  made  from  simple  inspection  of  the  jugular  vein.  If  neces- 
sary, venous  tracings,  supplemented  by  the  atropine  test,  may  be  resorted  to. 

PROONOSIS. 

The  course  of  cases  suffering  from  the  Adams-Stokes  syndrome  is 
veiy  variable.  It  is  probable  that  many  cases  die  in  the  first  attack,  but 
the  condition  remains  undiagnosed  or  is  ascribed  to  coronary  sclerosis. 
It  is  not  unlikely  that  histological  examination  of  many  cases  of  sudden 
death  would  reveal  lesions  in  the  bundle  of  His  or  its  artery.  In  some 
cases  death  occurs  within  a  few  weeks  or  months  after  the  first  attack,  but 
in  very  many  the  heart-block  may  last  for  many  years,  with  or  without  dis- 
appearance of  the  syncopal  attacks.  Many  cases  of  Edes's  series  lived  seven 
or  eight  years  after  the  first  attack.  Osier's  case  lived  thirty  years  after 
the  onset  of  bradycardia,  and  seven  years  after  the  first  syncopal  attack. 


476  DISEASES   OF   THE   HEART    AND    AORTA. 

It  is  stated  that  the  pulse-rates  of  JuHus  Caesar  and  of  Napoleon  were 
abnormally  slow  (Napoleon's  being  sometimes  40,  but  at  Elba  50  to  55), 
and  that  the  epilepsy  of  the  latter  was  a  sign  of  the  Adams-Stokes  syndrome, 
but  this  is  not  proved.  However,  it  is  certain  that  the  presence  of  com- 
plete heart-block  is  compatible  with  ability  to  do  a  considerable  amount  of 
work.  Vigouroux  had  under  observation  a  laborer  with  complete  heart- 
block  who  during  five  years  did  hard  work,  driving  a  cart  with  six  oxen  in 
the  hottest  weather.  His  heart  always  beat  at  a  rate  of  20.  Dr.  Archibald 
Hewan  was  able  to  climb  a  mountain  several  thousand  feet  high  when  his 
pulse  ranged  from  32  to  40  and  never  rose  above  the  latter.  Most  of  the 
cases  die  in  the  attacks  (Edes),  but  death  from  coronary  sclerosis  without 
Adams-Stokes  syndrome,  as  in  our  case,  is  not  uncommon.  Gerhardt  has 
recently  reported  three  cases  in  which  not  only  the  syncopal  attacks  but 
also  the  heart-block  completely  disappeared,  owing  to  subsidence  of  the 
pathological  process  in  the  auriculoventricular  bundle  which  was  not 
totally  destroyed.  Prof.  Thayer's  case,  quoted  above,  probably  belongs  to 
this  group. 

TREATMENT. 

As  regards  treatment  it  must  be  frankly  admitted  that  there  is  no 
drug  at  our  disposal  which  either  improves  conductivity,  prevents  stoppage 
of  the  ventricles,  or  increases  the  ventricular  rate. 

General  experience  has  shown  that  digitalis  is  either  without 
effect  or  positively  harmful,  and  v.  Tabora  has  shown  experi- 
mentally that  it  both  decreases  conductivity  and  increases  the  period 
of  stoppage. 

Caffeine,  theobromine,  strychnine,  strophanthus,  and  amyl  nitrite 
are  equally  without  effect  upon  either  of  these  phenomena  in  both  clinical 
usage  and,  as  the  writer  has  found,  in  experimental  heart-block  in  dogs. 
Atropine  is  usually  without  effect,  but  may  be  of  temporary  benefit 
in  certain  cases  with  a  neurogenic  element  (as  in  those  of  Gibson  and 
Ritchie  and  Thayer).  August  Hofmann  reports  a  case  in  which  inhalations 
of  oxygen  were  of  distinct  benefit,  but  in  the  writer's  experience  this  is 
not  often  the  case.  Ammonium  carbonate,  with  which  Burnett  claimed 
to  have  aborted  attacks,  has  not  been  much  used  in  recent  years. 

In  the  syphilitic  cases,  however,  antiluetic  treatment  — 
inunctions  of  mercury  and  administration  of  large  doses  of 
potassium  iodide,  ascending  to  4  Gm.  (5j)  t.i.d.,  by  mouth — has 
been  known  to  bring  about  a  cure  by  absorption  of  the  gummatous 
lesion  (Schmaltz,  Erlanger),  and  should  be  tried  whenever  there  is  a 
suspicion  of  lues. 

Peculiar  postures  sometimes  help  in  warding  off  syncopal  attacks 
by  improving  cerebral  blood  flow  until  the  ventricular  rhythm  has  become 
established.  Stokes  (1846)  writes  that  his  patient  "had  two  threatenings 
of  fits  since  his  admission,  and  warded  both  off  by  a  peculiar  manoeuvre:  as 
soon  as  he  perceives  symptoms  of  the  approaching  attack  he  directly  turns 
on  his  hands  and  knees,  keeping  his  head  low,  and  by  this  means  he  says 
he  often  averts  what  otherwise  would  end  in  an  attack."  This  was  the 
patient's  physiological  therapy  to  prevent  cerebral  anaemia. 


HEART-BLOCK   AND   ADAMS-STOKES   SYNDROME.       477 

It  is  evident  that  we  have  no  specific  remedy  or  procedure  for  the 
relief  of  the  Adams-Stokes  syndrome.  Nevertheless,  since  most  cases 
live  several  years  after  the  first  attack,  a  good  deal  can  be  done  for  the 
patient.  The  two  aims  to  be  kept  in  view  are,  first,  to  avoid  anything 
which  brings  on  rapid  changes  of  pulse-rate  (excitement,  emotion,  exertion, 
straining  at  stool) ,  and,  second,  to  enable  the  ventricles  to  gain  their  inher- 
ent rhythmicity  and  thus  obyiate  stoppage.  As  has  been  seen  from  Schuster 
and  Prentiss's  case  and  from  the  effect  of  exercise  in  Erlanger's  case,  exer- 
cise is  a  particularly  potent  factor  in  bringing  on  attacks  in  the  early  stage 
of  the  disease.  Absolute  rest  is  therefore  indicated  as  long  as  the  pulse- 
rate  is  at  all  unstable  {i.e.,  when  there  is  transition  from  partial  to  complete 
block)  and  vice  versa. 

When  complete  block  has  become  permanent  (for  at  least  several 
weeks)  the  condition  is  quite  different.  The  ordinary  influences  (emotion, 
mild  exercise,  etc.)  affecting  auricular  rate  now  no  longer  play  a  role,  and 
the  attack  seems  to  be  chiefly  due  to  the  action  of  COj  upon  the  ventricular 
muscle,  as  in  holding  the  breath  after  exercise,  or  in  the  similar  phenomena 
when  straining  in  order  to  lift,  void,  or  defecate.  In  the  stage  of  complete 
block  the  patient  may  therefore  be  gradually  allowed  exercise  which  does 
not  cause  him  exertion.  He  must  learn  to  avoid  the  latter,  since  it  may 
bring  him  sudden  death. 

In  all  stages  of  the  disease  the  bowels  should  be  kept  open  and  the 
stools  fluid,  but  excessive  purgation  and  straining  at  stool  should  be  avoided. 

Moreover,  it  should  not  be  forgotten  that  in  a  certain  number  of  cases, 
like  that  of  J.  L.  (page  467)  and  those  of  Gerhardt  mentioned  above,  the 
entire  process  may  be  due  to  acute  toxic  or  myocarditic  changes 
and  may  be  transitory,  so  that  if  the  patient  be  kept  at  rest  during  the 
acute  period  the  whole  inflammatory  process  in  the  auriculoventricular 
bundle  may  subside  and  perfect  health  may  return,  whereas  strain  upon 
the  heart  may  prevent  the  inflammatory  process  from  subsiding  and  may 
cause  the  attacks  to  continue. 

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Butler,  G.  R.:  Heart-block  (Adams-Stokes  Disease),  Am.  J.  M.  Sci.,  Phila.  and  N.  Y., 

1907,  cxxxiii,  715. 

Gerhardt,     D.:  Ueber     Riickbildung    des     Adams-Stokes'schen     Symptomenkomplexes, 

Deutsch.  Arch.  f.  khn.  Med.,  Leipz.,  1908,  xUii,  485. 
Edes,  R.  T.:  Slow  Pulse,  with  Especial  Reference  to  Stokes- Adams  Disease,  Trans.  Asso. 

Am.  Phys.,  Phila.,  1901,  xvi,  521. 
Thanhoffer:  Centralbl.  f.  d.  Med.  Wissensch.,  1875,  405.    Quoted  from  His. 
Neuburger,  Th.,  and  Edinger,  L.:  Einseitiger  fast  tot  aber  Mangel  des  Cerebellums,  Varix 

oblongatae  Herztod  durch  Accessoriusreizimg,  Berl.  klin.  Wchnschr.,  1898,  xxxv,  69. 
Gibson,  G.  A.,  and  Ritchie,  W.  T.:  Further  Observations  on  Heart-block,  Practitioner, 

Lond.,  1907,  i,  587. 
Mackenzie,  James:  New  Methods  of  Studying  the  Affections  of  the  Heart,  Brit.  M.  J., 

1905,  i,  519,  587,  702,  759,  812. 
Powers.     Quoted  from  Edes. 

Saigo,  Y.:  Die  Purkinjeschen  Muskel  fasem  bei  Erkrankungen  des  Myokards,  Verh.  d. 

Deutsch.  path.  Ges.,  Jena,  1908,  xii,  165. 
Dunn,  A.  D.:  Atrioventricular  Dissociation  following  Diphtheria,  J.  Am.  M.  Asso.,  Chicago, 

1908,  ],  1985. 

Strubing:  Deutsch.  med.  Wochnsch.,  Leipz.,  1893.    Quoted  from  Edes. 

Hewlett,  A.  W.:  Digitalis  Heart-block,  J.  Am.  M.  Asso.,  Chicago,  1907,  xlviii,  47. 

Gibson,  A.  G.:  The  Action  of  DigitaUs  on  the  Human  Heart,  Quart.  J.  M.  Sc,  Oxford, 

1907,  i,  173. 
Deneke:  Zur  Rontgendiagnostik  seltener  Herzleiden,  Deutsch.  Arch.  f.  klin.  Med.,  Leipz., 

1906,  Ixxxix,  39. 
Einthoven,  W.     Quoted  on  page  61. 

Schreiber,  E.:  Ueber  Herzblock  beim  Menschen,  ibid.,  1906,  Ixxxix,  277. 
Vigouroux:  Gaz.  d.  hop..  Par.,  1876.    Hewan,  A.    Quoted  from  Edes. 
Schmaltz:  Zur  Kenntniss  der  Adams-Stokes'scher  Krankheit,  Miinchen.  med.  Wchnschr., 
1905,  lii,  1120. 


XII. 

PERICARDITIS. 

Historical. — The  presence  of  changes  in  the  pericardium  in  animals 
was  known  to  Galen,  and  Senac  in  1749  described  the  condition  in  man. 
Auenbrugger  and  later  Corvisart  were  able  to  make  out  changes  in  dul- 
ness  due  to  pericardial  effusions.  Laennec  detected  the  murmur  of  fibrin- 
ous pleurisy,  and  described  it  as  resembling  the  creaking  of  a  new  saddle, 
but  its  diagnostic  significance  was  positively  established  by  Colhn  and  by 
DevilUers  in  1824. 

ETIOLOGY. 

The  frequency  with  which  pericarditis  occurs  varies  greatly  according 
to  various  observers,  and  particularly  according  to  the  age  of  their  patients. 
It  seems  to  be  considerably  more  common  in  children  than  in  adults  with 
cardiac  disease,  as  stated  by  Poynton,  as  it  accompanied  endocarditis 
and  myocarditis  in  94  per  cent,  of  Sturges's  cases  of  heart  disease  (carditis) 
from  the  Great  Ormond  Street  Children's  Hospital.  This  is  in  accordance 
with  the  somewhat  exaggerated  statement  of  Cadet  de  Gassicourt  that  all 
children  who  are  killed  by  rheumatism  die  from  pericarditis;  but  it  applies 
more  to  children  of  the  second  decade  than  of  the  first,  since  death  from 
rheumatic  affections  is  most  common  in  the  second  decade.  Pericarditis 
was  found  in  19  of  Osier's  73  autopsies  upon  cases  of  chorea.  Pericar- 
ditis occurred  in  230  (1  per  cent.)  of  the  cases  admitted  to  the  medical 
service  of  the  Johns  Hopkins  Hospital.  Of  these  53  were  associated  with 
endocarditis;  8  with  myocarditis.  Other  factors  were  pneumonia  39; 
rheumatism  31;  nephritis  33;  tuberculosis  25;  pleurisy  17;  gonorrhcea  3; 
aneurism  2;  leukaemia  2;  syphilis  1.  Rheumatism  occurred  in  51  per  cent, 
of  the  100  cases  reported  by  Sears  from  the  Boston  City  Hospital.  This 
relationship  between  pericarditis  and  rheumatism  has  been  proved  experi- 
mentally by  Wasserman,  Triboulet,  Poynton  and  Paine,  Walker,  Cole  and 
Beattie  (page  301). 

Pneumonia  is  also  one  of  the  common  causes  of  pericarditis  (18  per 
cent,  of  Sears's  series),  and  usually  ranks  next  to  the  rheumatic  cycle  as  an 
etiological  factor.  Pericarditis  was  present  in  4.66  per  cent,  of  the  cases  of 
pneumonia  at  the  Johns  Hopkins  Hospital  (Chatard),  and  in  2-3  per  cent, 
of  Preble's  series  in  Chicago.  According  to  the  latter  observer  its  relative 
frequency  is  about  proportional  to  the  extent  and  severity  of  the  disease. 
This  claim  is  also  borne  out  by  Chatard's  statistics  (frequency  of  15.7  per 
cent,  in  the  cases  coming  to  autopsy).  Moreover,  the  appearance  of  an 
acute  pericarditis  in  the  course  of  the  disease  is  a  very  grave  sign,  for 
only  two  cases  (6.5  per  cent.)  of  Chatard's  series  recovered. 
480 


PERICARDITIS.  481 

Pericarditis  is  also  common  in  scarlatina  (especially  with  strepto- 
coccus infection),  in  severe  measles,  and  in  smallpox.  In  the  latter  it  is 
frequently  purulent. 

Tuberculous  pericarditis  is  quite  common  (8  per  cent,  of  Breitung's 
autopsies),  and  in  contrast  to  the  rheumatic  form  rarely  subsides.  It  often 
ends  in  effusion. 

The  pericarditis  of  chronic  nephritis  and  uraemia  constitutes  a  frequent 
termination  of  this  disease,  though  it  is  by  no  means  always  fatal.  It  is 
usually  due  to  an  intercurrent  infection,  and  the  pyogenic  cocci  can  often 
be  cultivated  from  the  exudate. 

Pericarditis  may  also  result  as  a  secondary  infection  in  septicaemia  and 
in  puerperal  infections  as  well  as  in  gonorrhoea,  especially  when  there  is 
accompanying  arthritis.  It  is  rare  in  typhoid  fever  (3  times  in  McCrae's 
1500  cases) ;  occurs  occasionally  in  influenza;  and  sometimes  results  from 
septicaemias  due  to  B.  coli,  B.  aerogenes  capsulatus,  B.  pyocyaneus,  etc. 

Trauma  without  direct  injury  of  the  pericardium  or  viscera  was  the 
cause  of  pericarditis  in  Blancard's  case  in  1688,  and  a  large  number  of  cases 
due  to  this  cause  were  collected  by  Bernstein  in  1896.  Blows  upon  the  chest, 
wagon  running  over  the  body,  etc.,  are  the  common  causes. 

FORMS    OF    PERICARDIAL    EXUDATION. 

The  exudate  into  the  pericardial  cavity  may  assume  various  forms. 
In  simple  venous  stasis  and  asphyxia  of  the  endothelial  cells  (hydro- 
pericardium)  a  clear  thin  fluid  of  low  specific  gravity,  relatively  poor  in 
proteid  and  especially  in  fibrinogen,  is  secreted.  When  there  is  true  inflam- 
mation of  the  pericardium,  the  exuded  fluid  is  rich  in  fibrinogen  and  of  rela- 
tively high  specific  gravity  (over  1015)  and  contains  nucleo-albumen 
(clouding  with  acetic  acid).  Samuel  has  shown  that  when  the  exudate  is 
poor  in  fibrin  ferment  it  remains  fluid  (pericarditis  with  effusion) ,  whereas 
when  this  is  present  the  fibrinogen  coagulates  (fibrinous  pericar- 
ditis). According  to  Opie,  the  enzymes  are  derived  chiefly  from  the 
leucocytes,  especially  the  polymorphonuclears,  and  hence  the  amount  of 
fibrin  deposited  depends  largely  upon  the  number  of  these  cells  present. 
Moreover,  since  these  cells  pass  out  from  the  blood-vessels,  the  fibrin  is  first 
and  most  thickly  deposited  in  the  vicinity  of  the  latter, — i.e.,  along  the 
epicardium  above  the  circumflex  and  descending  rami  of  the  large  coronary 
arteries,  where  it  begins  in  the  form  of  strands  passing  out  from  about 
the  leucocytes,  and  hence  gives  the  heart  a  shaggy  appearance  (cor  villosum. 
Fig.  279).  This  layer  of  fibrin  usually  has  the  appearance  and  consistency 
of  a  yellow  batter.  When  fresh  it  is  not  very  adherent  to  the  heart,  and 
may  reach  a  thickness  of  an  inch  or  more.  There  may  be  no  fluid  in  the 
pericardial  cavity,  but,  as  a  rule,  both  fibrin  and  fluid  are  present,  the 
latter  often  in  large  quantities.  The  fluid  is  usually  thick,  containing 
uncoagulated  fibrinogen  as  well  as  small  flaky  masses  of  fibrin,  which  may 
render  it  too  thick  to  be  removed  by  aspiration.  W^hen  the  exudate  is 
extremely  rich  in  bacteria  and  leucocytes,  the  proteolytic  enzymes  are 
given  off,  which  digest  the  fibrin,  and  the  fluid  becomes  purulent. 

W'hen  the  fibrinous  exudate  of  a  simple  pericarditis  is  absorbed  rapidly, 
it  leaves  no  traces  and  the  pericardium  again  becomes  clear.    But  when  it 

31 


482 


DISEASES   OF   THE   HEART    AND    AORTA. 


lasts  for  some  time  and  the  resolution  is  slow,  organization  takes  place, 
and  white  patches  of  pericardial  thickening  ("milky  spots")  are  found 
over  the  surface  of  the  heart. 

These  may,  however,  result  from  small  perivascular  foci  like  those  of 
chronic  myocarditis,  without  ever  giving  rise  to  the  clinical  picture  of 
pericarditis. 


Fig.  278. — Acute  fibrinous  pericarditis. 


Fir.  279. — Tuberculous  pericarditis  (cor  villosum'). 


Organization  and  Adhesion. — The  strands  of  newly  formed  connective 
tissue  may  penetrate  the  fibrin  between  the  two  layers  of  pericardium  and 
completely  bridge  the  cavity  with  fibrous  strands  (Fig.  286).  In  many 
cases  the  tug  of  the  heart  in  systole  stretches  these  out  into  fibrous  cords 
an  inch  or  more  in  length;  in  other  cases,  or  over  other  parts  of  the  same 
heart,  the  adhesions  are  denser,  the  two  surfaces  may  be  completely  glued 
together  and  the  cavity  obhterated  (adherent  pericardium). 

The  division  into  these  forms  of  pericarditis  is,  therefore,  an  arbitrary- 
one,  but,  as  will  be  seen,  is  made  necessary  by  the  absolute  difference  in 
both  diagnostic  signs  and  mechanical  effects  upon  the  circulation,  and 
thus  as  regards  indications  for  treatment.  Their  relative  frequency  is 
shown  in  the  following  table,  which  Gibson  quotes  from  Breitung's  autop- 
sies at  the  Berlin  Charite  Hospital  (Virchow's  Department). 

Cases.  Per  cent. 

Serofibrinous 108  33.3 

Hemorrhagic 30  9.2 

Purulent 24  7.5 

Tuberculous  (secondary) 24  7.5 

Tuberculous  (primary) 2  0.7 

Partially  adherent .111  34.3 

Totally  adherent 23  7.3 

Ossified 2  0.7 

324  100 


PERICARDITIS.  483 

Although  the  pathogenesis  is  the  same,  the  chnical  manifestations  of 
fibrinous  pericarditis,  pericardial  effusion,  and  adherent  pericardium  are 
different;  hence  they  are  discussed  separately. 

SIMPLE  FIBRINOUS  PERICARDITIS. 
PATHOLOGICAL    PHYSIOLOGY. 

The  friction  due  to  the  presence  of  the  fibrinous  exudate  imposes  a 
slight  increase  in  the  resistance  to  both  contraction  and  filling  of  the  heart. 
The  exudate  itself  takes  up  a  certain  amount  of  space  in  the  pericardial 
cavity  and  may  thus  somewhat  diminish  the  filling  of  the  heart;  but 
these  factors  rarely  suffice  to  embarrass  the  circulation. 

Either  as  a  result  of  the  accompanying  injury  to  the  heart  muscle  or 
from  irritation  of  the  depressor  nerve,  the  peripheral  vessels  are  dilated 
and  the  blood-pressure  is  low.  The  pulse  also  becomes  small  and  rapid, 
but  is  usually  regular. 

SYMPTOMS. 

Precordial  pain,  palpitation,  shortness  of  breath,  and  weakness  are 
the  common  complaints,  as  well  as  occasional  chilly  feelings.  Fever,  with 
which  these  are  associated,  is  generally,  but  not  always,  present. 

The  onset  is  very  often  insidious,  and  the  disease  may  not  be  recog- 
nized at  all  by  the  patient.  Precordial  pain  is  the  most  striking 
symptom.  Sibson  estimates  that  it  occurs  in  70  per  cent,  of  the  cases. 
Henry  Head  calls  attention  to  the  fact  that  the  pain  of  pericarditis  is  not 
a  referred  pain,  but  a  true  local  pain,  often  limited  to  the  area  over  which 
the  friction  is  audible  and  associated  with  tenderness  on  pressure  and  on 
percussion.  It  does  not  radiate  from  this  site,  and  differs  in  this  respect 
from  the  anginal  pain.  The  other  symptoms,  shortness  of  breath  and  palpi- 
tation, manifest  no  special  peculiarity. 

Occasionally,  especially  when  the  pericarditis  affects  the  posterior 
wall  of  the  pericardium,  there  is  pain  on  swallowing.  This  pain 
is  in  every  way  similar  to  the  tenderness  of  the  interspaces  in  front,  and 
occurs  when  the  bolus  of  food  presses  upon  the  pericardium  as  it  passes 
down  the  oesophagus. 

When  the  recurrent  laryngeal  nerve  is  affected  by  the  inflammation, 
aphonia  or  change  in  the  voice  results.  Involvement  of  the  phrenic 
often  produces  hiccough. 

PHYSICAL    SIGNS. 

The  patients  are  usually  quite  pale,  occasionally  cyanotic.  Except 
for  accompanying  joint  involvement,  fibrinous  pleurisy,  or  pulmonary 
consolidation,  there  are  few  signs  outside  the  heart.  QCdema  of  the  extremi- 
ties is  rare  unless  there  are  accompanying  valvular  lesions.  Over  the  heart 
there  may  be  some  precordial  bulging,  especially  in  children,  but  the  cardiac 
impulse  may  be  less  marked  than  usual,  weak,  diffuse,  and  wavy.  On 
palpation  there  is  sometimes  a  slight  superficial  scratching  felt,  especially 
between  the  left  parasternal  line  and  the  sternum;  but  this  is  by  no  means 
as  marked,  as  frequent,  or  as  regular  as  in  valvular  lesions. 


484  DISEASES   OF  THE   HEART    AND    AORTA. 

The  area  of  cardiac  dulness  and  flatness  may  or  maj'  not  be  increased 
in  one  or  both  directions,  dependent  upon  the  amount  of  the  exudate  as 
well  as  upon  the  degree  of  dilatation  of  the  heart,  but  the  outlines  char- 
acteristic of  pericardial  effusion  are  not  present  when  the  exudate 
is  plastic. 

The  pathognomonic  sign  of  fibrinous  pericarditis  is  the  superfi- 
cial scratching  or  churning  murmur  or  fri cation  sound 
described  by  Laennec  as  resembUng  the  rubbing  of  a  new  saddle.  It 
can  be  imitated  more  or  less  closely  by  placing  the  palm  of  the  hand  over 
the  ear  and  then  scratching  to  and  fro  upon  the  back  of  the  hand  with  the 
finger-nail.  The  pericardial  friction  is  exactly  similar  in  character  to  the 
friction  heard  in  pleurisy,  but  its  time  is  coincident  with  the  cardiac  cycle. 
It  does  not,  however,  coincide  sharply  with  either  systole  or  diastole,  but 
is  usually  heard  during  portions  of  both.  It  is  usually  louder  during  systole 
than  during  diastole,  probably  because  the  two  surfaces  are  moved  across 
one  another  with  greater  force.    A  short  pause  usually  occurs  between  the 

systolic  and  the  diastolic  portion 


of  the  friction.  The  diastolic 
friction  is  softer  than  the  systolic, 
occurs  rather  early,  and  ceases 
during  the  latter  half  of  this 
period,  or  in  other  words  as  ven- 
tricular filling  diminishes.  It 
Fig.  280.-Diagram  showing  the  relations  of  the       may  also  be  heard  again  at  the 

pericardial  and  pleural  frictions  to  the  cardiac  and  time    of    auricular    Systole,    giving 

respiratory  movements.     The  pericardial  friction  is  4.   •    i  1      x         i.u         r  •    a* 

indicated  by  narrow  zigzag  line,  the  pleural  friction  a     triple     SOUncl     tO     the      iriCtlOn 


■nMvcimiajMii 


•MKLARDIAI.               „n,J\|s       ,«|'^I\,    . 

„rv.i\ 

i\r^  _i^K 

puufun.              kit     lit.. 

.   .   i   AAAik 

fBlCnON             -    -    • 

,..IM\ 

.JM^l  A-TilAV 

bLklSids"*''^^^'  *^^  ''^'"^  ^'^''^  ^^'  ^'^^  "^"^^  (Broadbent).  Sometimes,  espe- 
cially when  the  pericarditis  is  just 
beginning  and  the  friction  very  soft,  it  is  not  heard  at  all  during  diastole. 

The  friction,  as  a  rule,  does  not  replace  the  normal  heart  sounds,  but 
these,  as  well  as  loud  endocardial  murmurs,  may  be  heard  simultaneously 
with  it.  Their  more  distant  quahty  tends  to  accentuate  the  superficiality 
of  the  friction  sound.  Moreover,  the  latter  is  considerably  accentuated 
by  moderate  pressure  of  the  stethoscope  in  the  interspaces.  As  Emerson 
has  shown,  this  is  also  true  of  certain  endocardial  sounds,  but  the  latter 
are  quite  different  in  quality  from  a  fresh  pericarditis. 

As  the  exudate  is  absorbed,  the  friction  softens  gradually  into  a  barely 
distinguishable  roughening  of  the  first  sound,  and,  finally,  disappears 
altogether. 

When  portions  of  the  exudate  become  organized  and  remain  as  thick- 
enings of  the  endocardium,  they  may  still  give  rise  to  some  roughening 
of  the  first  sound,  which  may  be  very  difficult  to  interpret,  and  this  is 
especially  true  when  they  remain  in  the  form  of  fibrous  strands  and  loose 
adhesions  (see  page  500). 

The  friction  is  usually  first  heard  over  the  third  and  fourth  left  inter- 
space near  the  sternum,  over  the  area  at  which  the  exudate  first  appears. 
In  the  cases  which  are  secondary-  to  pneumonia  and  pleurisy  there  is  often 
a  "pleuroperi  car  dial"  friction,  with  respiratory^  accentuation 
heard  over  a  considerable  strip  along  the  left  margin  of  the  heart  where 


PERICARDITIS.  485 

the  pleura  overlies  the  pericardium.  The  pleurisy  exists  in  the  layers  of 
pleura  in  front  of  the  pericardium.  The  two  processes  exist  simultaneously 
in  separate  cavities  whose  walls  are  in  contact.  Sears  has  pointed  out 
that  in  recurrent  attacks  of  pericarditis  the  friction  may  be  heard  only 
at  the  back  in  the  left  interscapular  region.  This  occurred  in  a  case  in 
which  the  anterior  portion  of  the  pericardium  was  adherent.  The  pulse 
in  acute  pericarditis  is  usually  small  and  rapid,  the  blood-pressure  low 
(100  mm.  or  under),  and  the  pulse-pressure  small  (10-25  mm.),  but  this  is, 
at  least  in  part,  due  to  the  loss  of  vasodilator  tone,  and  in  part  to  the  myo- 
cardial weakening  brought  about  by  the  same  process. 

DIAGNOSIS, 

Diagnosis  is  usually  simple,  and  the  murmurs  are  rarely  mistaken  for 
endocardial,  although  Osier  mentions  one  case  in  which  a  to-and-fro  aortic 
murmur  was  mistaken  for  a  pericardial  rub. 

When  a  certain  amount  of  fluid  is  present  in  the  pericardium  the 
friction  may  disappear  if  the  heart  is  pushed  backward;  and,  as  a  small  peri- 
carditial  effusion  is  often  overlooked,  the  whole  condition  may  escape 
diagnosis. 

Case  of  Simple  Fibrinous  Pericarditis. 

F.  G.,  a  colored  hod-carrier,  aged  50,  entered  the  Johns  Hopkins  Hospital  on  July  22, 
1904,  complaining  of  pain  around  the  heart.  Except  for  the  fact  that  one  son  died  of  gal- 
loping consumption,  the  family  history  is  negative. 

The  patient  has  been  a  healthy  man,  but  had  measles,  chicken-pox.  whooping-cough, 
mumps,  scarlet  fever  as  a  boy,  and  rheumatic  fever  at  38.  He  is  not  subject  to  sore 
throat.  He  had  a  cough  with  pain  in  the  chest  twenty  years  before  admission,  but 
has  had  no  recurrence.  He  has  had  several  attacks  of  gonorrhoea.  He  has  always 
done  hard  work. 

He  was  perfectly  well  until  six  weeks  before  admission,  when  he  had  severe 
pain  in  the  right  thigh  and  h  i  p  which  lasted  five  weeks,  but  he  kept  at  work 
in  spite  of  the  pain.  Four  days  before  admission  he  began  to  cough,  and  two  days  later 
felt  a  cutting  pain  around  the  heart,  which  was  especially  severe  on  drawing 
a  deep  breath.  This  has  persisted.  He  did  not  notice  any  special  shortness  of  breath,  and 
kept  at  work  for  three  days  after  the  precordial  pain  had  set  in. 

The  examination  note  by  Dr.  Cole  states  that  the  patient  is  a  well-nourished  colored 
man,  mucous  membranes  of  fair  color,  no  glandular  enlargement.  Lungs  clear  throughout 
on  auscultation  and  percussion.  Over  the  heart  a  feeble  impulse  is  seen  in  the  fifth  left 
interspace  8.5  cm.  from  the  midline.  The  impulse  is  localized.  There  is  no  bulging  of  the 
interspaces.  On  percussion  the  area  of  cardiac  d  u  1  n  e  s  s  is  found  to  extend 
11.5  cm  .  to  the  left  of  the  midline  in  the  fifth  interspace,  .3.0  cm.  to  the  right  opposite 
the  fourth  rib.    The  cardiohepatic  angle  is  90°. 

The  heart  sounds  are  distinctly  heard  at  the  apex,  but  there  is  also  a  loud 
rough  pericardial  friction  which  is  not  exactly  synchronous  with  the  heart 
sounds  and  is  increased  by  pressure  with  the  stethoscope.  There  are  no  endocardial  mur- 
murs. The  friction  increases  in  intensity  toward  the  base  of  the  heart, 
where  the  heart  sounds  are  distant  and  the  second  pulmonic  is  louder  than  the  second 
aortic.     The  pulse  is  of  fair  volume,  moderate  tension,  regular,  88  per  minute. 

The  sputum  is  mucopurulent,  but  contains  no  tubercle  bacilli  and  no  elastic  fibres. 

Urine,  450  c.c,  amber  colored,  acid,  containing  a  con.siderable  amount  of  albumin 
and  numerous  hyaline  casts.  Blood  count  shows:  red  blood-corpuscles  3,500,000;  haemo- 
globin 50  per  cent.;  leucocytes  7100.     Temperature  ranges  from  101°  to  102.5°  F. 

An  ice-bag  was  kept  continuously  over  the  precordium,  and  he  was  given  strychnine, 
1.5  mg.  (iV  gr-)>  every  four  hours. 


486  DISEASES   OF   THE   HEART   AND    AORTA. 

On  the  second  day  after  admission  the  temperature  fell  to  normal  and  the  patient 
felt  better.  The  pain  in  the  chest  had  gone.  The  pericardial  friction  was  still  heard,  but 
less  intense  than  before,  and  by  the  following  day  could  be  heard  only  over  a 
small  area  in  the  fourth  left  interspace  near  the  sternal  margin. 
It  disappeared  entirely  during  the  course  of  the  following  week,  and  he  became  entirely 
well.  There  were  no  signs  of  pericardial  adhesion.  The  patient  left  the  hospital  on  August 
8,  in  the  third  week  after  his  admission,  and  has  not  sought  admission  since  then. 


TREATMENT. 

Absolute  rest  in  bed  is  necessary,  since  the  heart  must  be  spared  as 
much  as  possible,  and,  moreover,  cardiac  strain  and  venous  stasis  tend  to 
increase  the  exudation.  The  diet  should  be  light  or  should  consist  of  milk 
alone  during  the  acute  stages.  If  there  is  much  pain,  morphine  may  be 
freely  given  to  relieve  it,  since  this  symptom  is  not  likely  to  become  chronic; 
and,  on  the  other  hand,  it  is  important  to  keep  the  heart's  action  as  quiet 
as  possible.    For  this  purpose  an  ice-bag  is  usually  applied  to  the  precordium. 

Silva  has  shown  in  dogs  that  by  this  means  the  local  temperature 
within  the  pericardium  may  be  lowered  1°  or  even  3.5°  C.  (1.8° — 7.3°  F.). 
Buxbaum  states  that  the  use  of  the  ice-bag  in  pericarditis  is  now  quite 
general  throughout  the  world.  In  American  clinics  this  is  certainly  the 
case.  The  clinial  experience  of  the  writer  has  been  one  of  uniform  satis- 
faction in  its  use.  The  fact  that  Rubino  was  able  to  produce  pericarditis 
in  animals  by  the  intravenous  injection  of  cultures  of  pyogenic  cocci  only 
when  ice  was  simultaneously  applied  to  the  chest,  has 
probably  little  bearing  upon  the  therapeutic  use  of  the  latter,  since 
Rubino  probably  chilled  his  animals  severely,  while  in  the  therapeutic 
appUcation  the  cooling,  especially  of  the  deeper  layers,  is  both  localized 
and  mild.  No  doubt  the  local  temperature  of  the  inflamed  pericardium 
is  reduced  to  normal,  but  not  much  below  it. 

Other  methods  of  counterirritation  are  also  useful  and  devoid  of  this 
possible  objection.  Head  cites  a  case  in  which  relief  of  the  pain  within  five 
minutes  was  brought  about  by  the  application  of  three  1  e  e  c  h  e  s  to  the 
precordium,  and  Biers's  suction  cups  or  the  old-fashioned  dry  or  wet 
cupping  may  be  resorted  to  with  equal  satisfaction.  This  may  also  be  said 
of  hot  or  warm  poultices,  hot-water  bags,  and  the  modern  electrical  heating 
pads  whose  temperature  can  be  kept  regulated  with  great  accuracy.  Blis- 
ters (cantharides) ,  mustard  plasters,  Paquelin  cautery,  and  Finsen  light 
may  also  be  used  with  great  satisfaction,  or  even  a  ''light  bath" 
from  a  single  small  incandescent  lamp  with  reflector  placed  near  the  pre- 
cordium. 

Medicines  seem  to  be  of  little  value.  Caton  recommends  potassium 
iodide.  Broadbent  states  that  digitalis  should  be  avoided  in  the  early 
stages,  but  Romberg  recommends  its  use  in  the  cases  with  nephritis.  It 
should  be  used  at  once  and  should  be  preceded  by  intravenous  strophanthin 
if  signs  of  acute  cardiac  failure  manifest  themselves. 

The  pain  is  not  relieved  by  salicylates,  so  that  codeine,  .03  Gm.  (t^  gr.), 
heroin,  .005  Gm.  (yV  gr.)>  dionin,  .02  Gm.  (^  gr.),  or  morphine,  .016  Gm. 
(i  gr.),  must  often  be  given. 

•  The  bowels  should  be  kept  moving  easily  with  saline  purgatives. 


PERICARDITIS.  487 


PROGNOSIS. 

Osier  states  that  "simple  fibrinous  pericarditis  never  kills,"  but  peri- 
carditis is  frequently  seen  as  a  terminal  event  in  other  conditions,  espe- 
cially in  pneumonia,  tuberculosis,  gout,  and  nephritis.  In  any  of  these  it 
is  a  grave  but  not  always  fatal  sign. 

The  main  dangers  accompanying  fibrinous  pericarditis  are  the  develop- 
ment of  effusion  on  the  one  hand  or  of  pericardial  adhesions  on  the  other. 
Sometimes  all  three  conditions  occur  successively  in  the  same  case,  the 
fluid  collecting  within  a  few  days  after  the  fibrinous  exudate,  is  removed 
after  a  few  weeks  by  aspiration  or  absorption,  and  is  followed  by  organi- 
zation of  the  exudate  with  adhesions  which  usually  last  throughout  one  or 
several  years  and  finally  terminate  the  life  of  the  patient.  Fortunately, 
these  complications  are  by  no  means  the  rule,  and  in  many  cases  fibrinous 
exudate  is  absorbed  without  further  trouble. 

It  is  evident  from  both  the  pathological  and  the  clinical  stand-point 
that  the  fresher  the  exudate  the  cleaner  will  be  its  absorption.  Hence  the 
importance  of  vigorous  treatment. 

PERICARDITIS    WITH  EFFUSION. 

Frequently  during  the  course,  and  especially  in  the  second  or  third 
week,  of  an  acute  pericarditis  fluid  collects  within  the  pericardium.  Under 
normal  conditions  there  are  from  twenty-five  to  fifty  cubic  centimetres 
of  serous  fluid  present.  In  pericardial  effusions  from  500  c.c.  to  1  litre  is 
frequent;  as  much  as  4000  c.c.  has  been  found  at  autopsy  by  Verney.  A 
pericardial  membrane  of  the  usual  size  could  not  accommodate  so  large 
an  efi"usion,  and  stretching  of  the  former  usually  goes  on  simultaneously 
with  increase  in  the  latter.  Hence  it  follows  that  the  actual  size  of  the 
effusion  may  be  of  little  import,  and  a  small  rapidly  exuded  effusion  may 
produce  signs  of  intrapericardial  pressure  sooner  than  a  large  one  arising 
slowly. 

The  character  of  the  fluid  may  vary  as  much  as  its  quantity.  It  may 
be  thin  and  serous  and  free  from  coagula,  especially  when  poor  in  leuco- 
cytes, or  it  may  contain  small  gelatinous  coagula  forming  here  and  there 
about  masses  of  leucocj^tes;  or  this  process  may  be  so  generalized  that  the 
whole  mass  may  be  converted  into  a  very  thin  jelly.  Diapedesis  of  corpus- 
cles through  the  injured  vessel  walls  may  cause  it  to  become  bloodstained, 
a  condition  which  is  especially  frequent  in  carcinomatosis  or  sarcomatosis 
of  the  pericardium. 

PATHOLOGICAL    PHYSIOLOGY. 

Frangois-Franck,  Lagrolet,  and  Cohnheim  have  shown  that  the  injec- 
tion of  fluid  into  the  pericardial  cavity  hinders  the  entrance  of  blood  into 
the  auricles,  and  thus  causes  stasis  of  blood  in  the  vense  cavse  and  fall  in 
the  blood-pressure.  Their  experiments  were  repeated  by  Starling,  who 
found  that  on  injecting  successive  amounts  of  20  c.c.  and  10  c.c.  of  oil 
into  the  dog's  pericardium,  the  pressure  in  the  vena  cava  rose  gradually, 
while  that  in  the  aorta  and  pulmonary  vein  remained  constant  for  some 
time.     That  is  to  say,  the  rise  in  venous  pressure  compensated  for  the 


488 


DISEASES   OF   THE   HEART   AND    AORTA. 


increased  pressure  within  the  pericardium,  and  although  some  venous 
stasis  occurred  the  circulation  was  not  retarded.  As  much  as  60  c.c.  of  oil 
could  thus  be  injected  into  the  dog's  pericardium  without  producing  any 
other  change.  But  when  10  c.c.  more  were  injected  the 
condition  changed  suddenly  and  completely.  The  small  excess 
of  fluid  in  the  pericardial  cavity  had  caused  the  pressure  within  it  to  rise 
"considerably  above  that  in  the  veins,  and  above  the  level  to  which  the 
venous  pressure  could  rise  during  stasis.  The  walls  of  veins  and 
auricles,  therefore,  collapsed  under  excess  of  pressure 
(Fig.  281),  and,  since  but  little  blood  could  enter  the  ventricles,  the  blood- 


FiG.  281. — The  circulation  in  cases  with  pericardial  effusion.  (Diagrammatic.)  I.  Normal.  II. 
Small  effusion,  showing  the  rise  in  venous  pressure  and  the  increased  difficulty  in  the  filling  of  the  lieart. 
III.  Great  increase  in  intrapericardial  pressure,  showing  the  complete  cutting  off  of  venous  inflow  and 
fall  in  arterial  pressure.  The  area  shaded  with  horizontal  broken  lines  indicates  the  height  of  the  pressure 
within  the  pericardium. 

pressure  in  the  aorta  fell.  The  same  change  occurred  in  Frangois-Franck's 
experiments  when  the  intrapericardial  pressure  was  raised  from  10  mm.  to 
20  mm.  Hg.  When  the  pressure  was  not  relieved  death  ensued,  the  heart 
beating  for  a  short  time  after  the  circulation  had  ceased.  On  the  other 
hand,  when  the  small  excess  of  fluid  was  removed,  the 
blood -pressure  quickly  rose  again  and  the  circulation  returned 
to  normal.  This  experiment  exactly  reproduces  the  condition  in  man  when 
a  pericardial  effusion  is  collecting,  illustrates  the  mechanism  of  death  in 
that  condition,  and  also  illustrates  the  beneficial  effect  obtained  from  par- 
acentesis when  even  a  small  amount  of  fluid  is  removed. 


SYMPTOMS    AND    COURSE. 

Pericardial  effusion  is  somewhat  less  frequent  in  children  than  are 
the  other  forms  of  pericarditis,  its  subjects  being  usually  adults  and  often 
persons  past  middle  age.  The  .symptoms  of  pericardial  effusion  are  more 
insidious  than  those  of  the  fresher  fibrinous  inflammation,  pain  being 
somewhat  less  common  and  less  intense,  dyspnoea  and  weakness  being 
more  intense.  The  patients  are  very  much  more  comfortable  in  the  vertical 
than  in  the  horizontal  position,  the  difference  being  even  more  striking 
than  in  the  ordinary  forms  of  heart  disease.  Few  clinicians  indeed  can 
concur  in  James  Mackenzie's  statement  that  the  presence  of  fluid  in  the 


PERICARDITIS. 


489 


pericardium  does  not  give  rise  to  symptoms  of  circulatory  embarrassment. 
Fainting  spells  and  sudden  death  are  very  common,  occurring  when  the 
inflow  into  the  auricle  is  obstructed. 


PHYSICAL    SIGXS. 

The  patients  are  usually  pale  and  weak  with  rapid  respirations.  The 
veins  of  the  neck  and  extremities  may  be  prominent 
(high  venous  pressure),  and  this  is  especially  marked  when  the  intraperi- 
cardial  pressure  is  approaching  the  danger  point.  There  may  be  inspira- 
tory  distention  of  the  veins. 

Inspection  of  the  thorax  usually  shows  a  fulness  of  the  inter- 
spaces over  the  precordium,  and  frequently  a  very  diffuse  wavy  impulse 
which  is  lacking  in  the  definiteness  usually  seen  in  both  systolic  impulse 
and  systolic  retraction  over  and  about  the  normal  or  enlarged  heart. 
Neither  this  nor  the  presence 
of  a  cardiac  pulsation  outside 
the  apex  is  of  real  value  in 
establishing  the  diagnosis  of 
pericardial  effusion. 

Palpation,  as  a  rule,  reveals 
nothing  of  importance,  except 
that  the  cardiac  impulse  is 
usually   very  feeble   or  absent. 

Changes  in  Cardiac  Outline. 
—  The  pathognomonic  sign  is 
revealed  by  the  alteration 
of  dulness  on  percus- 
sion. Auenbrugger  in  his  first 
diagnostic  efforts  was  able  to 
demonstrate  a  great  increase  in 
cardiac  dulness  in  pericarditis 
with  effusion,  and  this  obser- 
vation was  confirmed  by  Cor- 
visart,  who  recognized  a  large 
area  of  flatness  in  the  form  of  a  triangle  with  base  downward.  This, 
however,  was  also  encountered  in  numerous  cases  of  dilated  heart  and 
led  to  many  errors  in  diagnosis,  until  T.  M.  Rotch,  of  Boston,  in  1878, 
demonstrated  that  flatness  ^^'as  present  in  the  fifth  right 
interspace  early  in  the  disease  and  constituted  an  almost  diagnos- 
tic feature.  He  was  able  to  prove  this  upon  the  cadaver  by  injecting 
various  quantities  of  cocoa  butter  into  the  pericardial  cavity.  Flat- 
ness in  the  fifth  right  interspace  appeared  whenever  more 
than  200  c.c.  of  cocoa  butter  had  been  injected.  Less  than  200  c.c. 
could  not  be  recognized. 

Rotch's  observations  were  confirmed  by  W.  Ebstein  in  1893,  who 
laid  stress  upon  the  obtuseness  of  the  angle  formed  by  cardiac  and  liver 
dulness  (cardiohepatic  angle).  This  dulness  is  particularly 
marked  when  the  patient  leans  forward  and  toward  the  right,  so  that  the 


Fig.  282. — Area  of  oardiac  dulness  from  pericardial 
effusion,  sliowing  Corvi.-^art  s  triangular  area  of  dulness 
and  Sibson's  pear-shapefl  area  of  flatness;  Rotch's  area 
of  dulness  (R)  in  the  fifth  right  interspace;  Ebstein 's 
obtuse  cardiohepatic  angle  (EB^i. 


490  DISEASES   OF   THE   HEART    AND    AORTA. 

fluid  gravitates  to  this  point.  The  right  border  of  an  enlarged  heart,  on 
the  other  hand,  always  forms  an  acute,  or  at  most  a  right,  angle  with  the 
liver  dulness,  and  flatness  rarely  extends  to  the  fifth  right  interspace, 
being  most  marked  in  the  fourth.  The  matter  has  been  still  further  investi- 
gated by  Aporti  and  Figaroli,  who  found  that  with  the  subject  in  the  ver- 
tical position  as  little  as  150  c.c.  of  fluid  showed  itself  by  pushing  the  area 
of  dulness  downward  and  outward  at  both  its  lower  angles — at  both  cardio- 
hepatic  angle  and  at  the  apex.  The  lower  border  of  flatness  is,  therefore, 
the  arch  with  concavity  downwards  which  had  already  been 
described  by  Concato.  When  more  fluid  collects,  the  pericar- 
dium becomes  more  tense,  all  the  surfaces  become  convex,  and  Concato's 
arch  disappears.  As  a  diagnostic  sign  the  variations  in  dulness  about  the 
apex  are  much  less  definite  than  in  the  fifth  right  interspace,  and  hence 
they  are  of  little  importance. 

At  the  upper  border  of  dulness  the  usual  slight  resonance  behind  the 
sternum  gives  way  to  a  tongue  of  absolute  flatness  when  the  exudate  is 
large,  so  that  the  dulness  assumes  the  form  of  a  pear  hang- 
ing from  its  stalk  (Sibson). 

Moreover,  the  pericardium  presses  upon  the  lungs  about  its  borders, 
causes  them  to  relax  and  give  rise  toSkodaic  tympany  and  tubu- 
lar breathing  not  only  in  front  but  also  at  the  angle  of  the 
left  scapula  (Ewart.)  Flatness  may  also  be  observed 
over  the  spines  of  the  vertebrae,  especially  from  the  fifth 
to  the  tenth,  where,  as  found  by  Koranyi,  the  note  is  normally  resonant. 
This  sign  may  also  be  present  when  the  left  auricle  is  greatly  dilated,  as 
in  mitral  insufficiency. 

Position  of  the  Heart  in  Pericardial  Effusion. — The  signs  on  auscultation 
may  vary.  Most  commonly,  as  found  by  Pirogoff  and  subsequent  writers, 
the  heart  sinks  in  the  pericardial  fluid  and  comes  to  lie  against  the  vertebral 
column  and  away  from  the  chest  wall,  from  which  it  is  separated  by  a 
thick  layer  of  fluid.  This  fluid  muffles  the  heart  sounds,  which  may  be 
totally  absent,  disappearing  first  about  the  apex,  later  at  the  base. 
Aporti  and  Figaroli  have  shown  that  with  650  c.c.  of  exudate  a  very 
small  area  of  heart  wall  near  the  base  will  still  remain  free  from  fluid,  and 
over  this  the  heart  sounds  and  friction  rub  may  be  heard. 

On  the  other  hand,  the  heart  sounds  and  friction  may  persist  even 
when  a  large  amount  of  fluid  is  present,  as  in  the  case  reported  below,  in 
which  the  pericardium  contained  1200  c.c.  of  fluid.  The  sounds  were  faint 
at  the  apex,  but  became  more  distinct  as  the  base  was  approached,  where 
the  friction  was  also  well  heard.  An  aspirating  needle  introduced  in  the 
sixth  left  interspace  came  at  once  against  the  heart.  At  autopsy  the  heart 
was  found  lying  against  the  chest  wall.  This  anterior  position,  though 
not  the  usual  one,  is,  according  to  Schaposchnikoff,  often  assumed  b}''  the 
heart  of  a  cadaver  when  fluid  or  paraffin  is  injected  into  the  pericardium. 
Schaposchnikoff  believes  that  the  heart  is  held  in  this  position  in  spite  of 
the  force  of  gravity  by  the  elasticity  of  the  great  vessels. 

Abdomen. — The  liver  may  be  both  enlarged  from  the  venous  stasis 
and  pushed  down  by  the  pericardial  effusion,  so  that  its  lower  edge  is  fre- 
quently palpable,  sometimes  even  as  low  as  the  umbilicus.     The  spleen 


PERICARDITIS. 


491 


may  also  be  somewhat  enlarged.  Ascites  and  movable 'dulness  are  some- 
times present. 

Over  the  extremities  the  veins  may  appear  distended,  and  there  is 
•often  oedema. 

Blood=pressure. — The  blood-pressure  is  usually  rather  low,  except  in 
the  cases  with  nephritis,  in  which  it  may  be  above  normal. 

The  pulse  is  usually  small,  frequently  collapsing,  and  often  of  the  type 
of  pulsus  paradoxus— fall  of  blood-pressure  during  inspiration,  with  de- 
crease in  the  size  and  frequency  of  the  pulse,  and,  on  the  other  hand,  inspi- 
ratory swelling  of  the  veins.  This  condition  is  due  to  traction  on  the  walls 
of  the  vena  cava  producing  stasis  during  inspiration. 


Fig.  283. — Positions  of  the  heart  in  pericarditi.*  with  effusion.  I.  The  fluid  is  in  front  of  the  heart, 
as  described  by  Pirogoff.  II.  The  heart  is  floated  up  against  the  chest  wall,  as  described  by  Schaposchni- 
koff.  ST,  sternum;  OE,  a-sophagus;  PV,  pulmonary  veins;  8,  eighth  thoracic  vertebra.  The  arrows 
infiicate  the  compression  of  the  auricles.     The  broken  line  indicates  the  outline  of  the  uncollapsed  auricle. 

X=ray  Examination. — Examination  with  the  fluoroscope  shows  the 
exact  size,  form,  and  position  of  the  effusion  (Fig.  283),  and  both  before 
and  after  paracentesis  may  be  of  great  help  in  locating  pockets  of  encapsu- 
lated fluid.  The  relations  to  the  diaphragm  and  the  presence  of  mediastinal 
adhesions  may  sometimes  be  diagnosed  by  this  means,  and  particularly 
by  means  of  permanent  radiographs  made  with  a  tube  of  low  vacuum. 


Case  of  Pericarditis  with  Effusiox. 

The  following  typical  case  was  under  the  writer's  care  in  the  Johns  Hopkins  Hospital. 
It  has  been  previously  reported  in  considerable  detail  by  Professor  Thayer. 

R.  C.  W.  B.,  a  German  saloon-keeper,  aged  59,  was  brought  to  the  hospital  at  12.30 
P.M.  on  Sept.  1,  1903,  barely  able  to  speak,  owing  to  shortness  of  breath  and 
"weakness.  He  was  too  ill  to  give  a  history,  except  for  the  statement  that  for  several 
years  he  had  been  troubled  with  shortness  of  breath,  which  has  gradually  increased  until 
the  past  few  days,  when  it  suddenly  became  very  much  aggravated. 

Examination  note  by  Dr.  Cole  was  as  follows:  Patient  is  a  moderately  well-nourished 
man,  muscles  flabby.  At  time  of  the  examination  he  is  lying  fiat  with  head  slightly  propped 
up  and  looks  very  ill.  Respiration  40  per  minute.  Pupils  are  small,  react  readily  to  light. 
Tongue  dry,  slightly  coated.  No  marked  pyorrhoea;  teeth  not  good.  Veins  of  the 
neck  are  very  full;  no  marked  pulsation  of  the  deeper  vessels.  No  general  glandular 
enlargement.  Chest:  Expansion  fairly  good;  equal;  considerable  respiratory  distress. 
Resonant  throughout  right  front  and  axilla  and  left  upper  front,  but  note  is  markedly 
impaired  in  lower  left  axilla  and  at  lower  right  back,  much  more  markedly  in  lower  left 


492 


DISEASES   OF   THE   HEART    AND    AORTA. 


back  up  to  the  angle  of  the  scapula.  On  auscultation. — Left:  Breath  sounds  are 
clear  throughout  upper  front  and  upper  back  except  for  a  few  mucous  rales  in  interscapular 
space.  Below  they  are  very  distant,  practically  absent  at  the  extreme  base,  except  just 
at  the  angle  of  the  scapula,  where  they  are  a  little  harsher  (Ewart's 
sign).  Right  side:  Breath  soimds  are  quite  clear  throughout  except  in  the  lower  back 
where  there  are  mucous  rales  and  breath  sounds  are  distant. 

Heart.  — There  is  no  impulse  visible  or  palpable.  There  is  a  wide  area 
of  cardiac  d  u  1  n  e  s  s  extending  above  to  the  middle  of  the  third  rib  16.5  cm. 
to  the  left  of  the  midline  in  the  fifth  interspace  when  the  patient  lies  on  his  right  side. 
When  on  his  back,  however,  the  dulness  is  difficult  to  make  out,  as  it  extends  directly  to 

the  dulness  in  the  axilla.  On  the  right 
dulness  extends  apparently  7  cm.  to 
the  right  of  the  midline  in  the  fourth 
interspace.  The  angle  between  the  upper 
limit  of  liver  dulness  and  the  cardiac  dul- 
ness is  very  obtuse.  There  is  quite 
definite  precordial  bulging,  though 
the  intercostal  spaces  seem  no  fuller  than 
on  the  right.  At  the  apex  and  over  the 
entire  precordium  the  heart  sounds 
are  barely  audible  until  one  reaches 
almost  to  the  costal  margin  in  the  fourth 
and  fifth  left  interspace,  where  the  sounds 
are  heard  faintly  with  a  to-and-fro  mur- 
mur, which  is  also  heard  over  the  sternum 
from  the  third  to  the  fifth  rib.  This 
m  u  r  m  u  r  is  quite  superficial  and 
is  louder  during  expiration  than 
(luring  inspiration,  apparently  not  increased 
liy  pressure  of  the  stethoscope.  It  sounds 
suspiciously  pericardial  in  charac- 
ter, but  not  definitely  so.  The  heart's 
action  is  almost  fetal  in  rhythm  (pulse- 
rate  138  per  minute).  Heart  sounds  are 
heard  more  loudly  in  the  second  left  inter- 
space; neither  aortic  nor  pulmonic  second 
is  specially  accentuated.  Pulse  is  very 
small   and  can  hardly  be  counted. 

The  abdomen  is  full.  There  is  no 
movable  dulness  in  the  flanks.  The  feet 
and  legs  are  markedly  oedematous. 

At  5.45  P.M.  the  patient  was  prepared 
for  paracentesis  pericardii  by  the  method 
of  Delorme  and  Mignon  under  aseptic  precautions.  An  incision  was  made  in 
the  fifth  left  interspace  at  the  sternal  margin,  the  pericardium  ex- 
posed, and  a  trocar  inserted  through  it.  By  means  of  a  Potain  aspirator  25-50  c.c.  of  thick 
serosanguineous  fluid  were  removed,  after  which  no  more  could  be  removed. 
Another  puncture  was  immediately  made  in  the  costoxiphoid  angle  and  a  small  amount 
of  fluid  again  removed.  The  patient's  pulse  and  general  condition  did  not  change.  He 
became  delirious  and  died  at  7.30  p.m. 

The  autopsy  findings  confirmed  the  clinical  observations.  There  were,  how- 
ever, still  1200  c.c.  of  pericardial  fluid  which  lay  behind  the  heart 
both  to  the  left  and  to  the  right.  The  heart  lay  directly  against  the 
chest  wall,  and  therefore  had  come  against  the  point  of  the  needle  and  prevented  the 
removal  of  the  fluid.  As  Dr.  Cole  remarked  in  a  subsequnet  note,  "the  fact  that  the  heart 
sounds  were  heard  loudest  over  the  sternum  and  along  the  left  sternal  margin  should  have 
led  me  to  insert  the  needle  either  to  the  right  of  the  sternum  or  far  to  the  left — outside  the 
mammillary  line"  (preferably  the  latter).  The  pericardium  was  lined  with  a  yellow 
fibrinous    exudate.      The  heart  muscle  showed  cardiosclerosis.     The    coronary 


Fig.  284. — Radiograph  of  a  patient  witli  pericar- 
dial effusion,  taken  with  the  tube  in  front  of  the 
patient.  (Kindness  of  Prof.  C.  M.  Cooper.)  The 
figure  shows  the  overflowing  of  the  pericardial  cav- 
ity. The  spots  over  tlie  surface  of  the  lungs  are 
artefacts  due  to  the  presence  of  air-bubbles  in  tlie 
developer. 


PERICARDITIS.  493 

c 

arteries  were  tortuous.  There  were  thickening  of  the  aortic  valves  and  adhesions  of  the 
cusps,  which  gave  rise  to  sUght  aortic  stenosis.  The  left  pleura  contained  700  c.c.  of  slightly 
turbid  straw-colored  fluid.  Both  lungs  contained  small  areas  of  tuberculous  broncho- 
pneumonia. 

PURULENT  PERICARDITIS. 

The  effusion  in  many  cases  is  purulent  and  associated  with  more  or 
less  severe  septic  symptoms,  septicaemia,  chills,  extreme  pallor  and  weak- 
ness, and,  as  a  rule,  a  septic  fever,  though  in  some  cases  the  temperature 
remains  normal. 

The  condition  may  follow  exposure  to  bad  weather,  empyema,  or 
trauma  to  either  the  front,  sides,  or  back  of  the  chest.  The  staphylococci, 
streptococci,  pneumococci,  gonococci,  and  a  great  variety  of  other  bacteria 
may  be  the  infective  agents. 

The  symptoms  and  physical  signs  are  very  similar  in  both  simple 
and  purulent  effusions.  The  history  of  trauma  and  the  presence  of  empyema 
or  other  foci  of  pus  speak  in  favor  of  a  purulent  effusion.  Leucocytosis 
may  be  present  in  both  conditions.  The  aspirating  syringe  usually  gives 
the  diagnosis. 

HYDROPERICARDIUM. 

Hydropericardium,  or  simple  serous  effusion  into  the  pericardium, 
may  occur  along  with  ascites,  hydrothorax,  and  general  anasarca  in  chronic 
heart  failure  or  in  nephritis,  or  it  may  occur  alone  as  a  result  of  local  venous 
stasis  from  the  pressure  of  mediastinal  growths,  glands,  or  aneurisms,  or 
from  strangulation  of  the  veins  by  adhesions.  In  this  case  an  afebrile 
course  is  run.  Leucocytosis  is  often  absent  (or  may  be  due  to  simultaneous 
bronchitis  or  bronchopneumonia),  and  the  diagnosis  rests  upon  the  signs 
of  the  intrathoracic  condition  which  is  the  causal  factor. 

The  differential  diagnosis  is  made  from  the  fluid  obtained  on  para- 
centesis, which  is  clear,  thin,  serous,  of  low  specific  gravity  (under  1018), 
and  gives  no  clouding  with  acetic  acid  indicative  of  nucleo-albumin.  It 
is  poor  in  leucocytes  and  fibrin  ferment,  and  there  is  not  much  albumin 
(shown  by  Esbach's  method).  The  presence  of  a  pericardial  friction  at 
any  time  during  the  course  of  the  disease  is  sufficient  to  exclude  a  simple 
hydropericardium. 

H^MOPERICARDIUM. 

Hsemopericardium  is  produced  by  the  effusion  of  pure  or  almost  pure 
blood  into  the  pericardium,  and  occurs  especially  as  a  result  of  direct  or 
indirect  trauma,  stab  or  gunshot  wounds  penetrating  the  cavity,  or  rupture 
of  the  heart  or  of  an  aneurism.  It  may  also  occur  from  erosion  of  a  blood- 
vessel by  a  malignant  growth. 

Hemorrhage  into  the  pericardium  takes  place  much  more  rapidly 
than  the  other  exudations,  so  that  the  pericardium  has  less  opportunity 
to  stretch  and  accommodate  itself  to  its  contents.  The  intrapericardial 
pressure,  therefore,  rises  more  rapidly  than  in  the  other  conditions,  and 
symptoms,  signs,  and  danger  develop  more  rapidly.  Death  may  occur 
at  once.  When  possible  operative  procedures  must  be  begun  promptly 
in  order  to  save  the  patient. 


494  DISEASES   OF   THE   HEART    AND    AORTA. 


PXEUMOPERICARDIUM. 

When  air  or  gas  enters  or  develops  within  the  pericardial  cavity  (as 
from  perforation  after  trauma  or  tuberculosis  or  infection  with  Bacillus 
aerogenes  capsulatus  Welchii  in  a  case  reported  by  Xicholls),  the  condition 
is  termed  pneumopericardium.  Usually  this  is  associated  with  the  pres- 
ence of  purulent  or  serous  fluid  (pyopneumopericardium,  pneumohydro- 
pericardium) .  Since  there  is  normally  a  negative  pressure  (^3  to  — 5  mm. 
Hg)  within  the  cavity,  it  follows  that  air  will  enter,  just  as  into  the  thorax 
(pneumothorax),  whenever  there  is  a  free  perforation  to  the  outside  or  to 
the  air-passages.  This  is  most  frequent  in  perforating  wounds,  but  occa- 
sionally occurs  as  the  result  of  tuberculosis  or  perforation  of  a  purulent 
pericarditis. 

The  signs  of  pneumopericarditis  are  very  characteristic.  The  percus- 
sion note  over  the  cardiac  area  may  vary  from  a  bell-like  tympany 
to  an  absolutely  wooden  flatness,  or  when  there  is  an  open- 
ing of  medium  size  a  cracked-pot  note  may  be  heard.  With  a  free  communi- 
cation to  the  outside  such  as  results  from  operation  upon  the  pericardium, 
however,  the  air  within  the  pericardium  is  not  set  into  vibration  by  the 
percussion  stroke  and  does  not  alter  the  note  at  all. 

On  auscultation,  except  in  the  latter  condition,  a  loud  churning 
''mill-wheel''  murmur  is  heard,  but  when  the  communication  is  a  free 
one  this  may  be  totally  absent. 

TUBERCULOUS  PERICARDITIS. 

Tuberculous  pericarditis  is  a  common  and  severe  condition.  The 
fibrinous  stage  is  somewhat  more  chronic  than  in  the  other  forms  of  peri- 
carditis, lasting  several  weeks  or  months,  and  often  resulting  in  the  forma- 
tion of  deposits  of  fibrin  (Fig.  256)  an  inch  in  thickness,  with  or  without 
the  presence  of  fluid.  Gray  tubercles  of  various  size  may  be  visible  within 
and  upon  the  surface  of  the  exudate,  but  frequently  they  may  not  be  pres- 
ent, and  the  bacilli  must  be  sought  for  histologically  op  by  guinea-pig 
inoculation. 

The  fluid  in  pericardial  effusion  is  frequently  blood  stained.  It  is 
occasionally  purulent  (Kast).  Tuberculous  pericarditis  is  most  commonly 
associated  with  other  tuberculous  processes,  especially  involvement  of 
the  pleurae,  but  it  may  also  occur  as  a  "primary"  manifestation  by  spreading 
from  caseous  mediastinal  lymph-glands. 

The  course,  though  more  chronic  than  other  pericardial  processes, 
is  quite  similar,  but  the  exudate  is  not  absorbed  completely  and  goes  on 
to  either  fluid  or  adhesive  pericarditis.  Frequently  both  conditions  occur 
and  encapsulated  effusions  result.  There  is  usually  a  considerable  rise  of 
afternoon  temperature. 

The  physical  signs  and  therapy  of  tuberculous  pericarditis  are  about 
the  same  as  in  the  other  forms,  plus  the  general  management  of  a  case  of 
tuberculosis — rest,  fresh  air,  very  liberal  diet  (when  cardiac  symptoms  have 
subsided) ,  and  sustaining  measures.    The  prognosis  is  bad. 


PERICARDITIS.  495 


TREATMENT  OF  PERICARDITIS  WITH  EFFUSION. 

Palliative  treatment  of  fluid  within  the  pericardium  must  be  limited 
to  the  periods  in  which  intrapericardial  pressure  is  well  below  the  range 
of  venous  pressure,  and  must  be  pursued  with  full  cognizance  of  the  fact 
that  death  may  eiisue  whenever  the  pressure  exceeds  this  limit. 

The  palliative  measures  consist  of  counterirritation,  with  ice-bag  or 
poultices,  etc.,  blisters,  and  especially  application  of  Bier's  suction  cups 
or  leeches.  Diuretics, — theocin,  diuretin, — combined  with  digitalis  or 
strophanthus,  and  free  purgation  may  be  resorted  to,  and  the  liquid  intake 
restricted  to  below  1000  c.c.  per  day,  in  the  hope  of  reducing  the  pericardial 
fluid  by  these  means.  However,  these  methods  are  at  best  but  feeble 
palliatives,  and  often  more  risk  is  entailed  in  their  use  than  in  the  more 
radical  procedures. 

Paracentesis  Pericardii. — The  idea  of  removing  fluid  within  by  tapping 
the  pericardium  was  first  suggested  in  1646  by  Riolan,  who  advised  tre- 
phining the  sternum  one  inch  above  the  xiphoid.*  He  did  not  attempt, 
however,  to  carry  it  out,  and  the  first  operation  upon  the  pericardium  was 
performed  in  1819  by  Romero,  of  Barcelona.  Romero  operated  upon  three 
cases  of  pericarditis,  with  two  recoveries,  a  percentage  which  is  above  the 
average  even  for  the  present  day.- 

Puncture  of  the  pericardium  by  means  of  a  trocar  was  first  performed 
by  Jowett,  of  Nottingham,  in  1827.  It  was  brought  into  more  general 
repute  by  Schuh,  of  Vienna,  under  Skoda's  direction  (1839),  in  France 
by  Trousseau  (1854)  and  by  Aran  (1855),  and  in  England  by  Clififord 
Allbutt  (1866).  Paracentesis  pericardii  should,  of  course,  be  undertaken 
with  all  possible  asepsis  of  skin,  hands,  and  instruments. 

The  instrument  used  has  varied  from  a  thick  trocar  several  millimetres  in  diameter 
to  the  finest  aspirating  needle.  The  ideal  cannula  is  one  which  has  a  bore  (about  1  mm.) 
sufficient  to  aljow  a  viscous  liquid  to  escape  easily,  and  yet  not  so  great  as  to  permit  the 
entrance  of  air  through  the  perforation.  A  trocar  and  cannula,  especially  one  ending  in 
a  T  and  stop-cock,  is  the  best  form  of  apparatus,  since  it  permits  the  operator  to  clear  the 
lumen  of  the  cannula  at  will  and  at  the  same  time  to  remove  the  fluid  by  suction  through 
an  aspirating  bottle.^ 

Various  sites  for  the  paracentesis  are  recommended,  with  four  ends 
in  view: 

1.  To  obtain  the  fluid. 

2.  To  avoid  infecting  the  pleural  cavity  and  puncturing  the  lungs. 

3.  To  avoid  puncturing  the  heart. 

4.  To  avoid  injuring  the  internal  mammary  artery. 

'  "  Si  non  passis  exhaurire  istud  serum  per  hydragoga,  licet  ne  terebra  sternum  aperire, 
intervallo  pallicis  a  cartilagine  xiphoide." 

^  It  is  interesting  that  this  method  has  recently  been  advocated  by  J.  H.  Bacon  (A 
Procedure  for  Opening  the  Pericardium,  Am.  J.  M.  Sc,  Phila.  and  N.  York,  1905,  cxxx, 
652)  as  a  result  of  a  series  of  experiments  upon  the  cadaver.  Bacon  does  not  mention  the 
work  of  these  pioneer  surgeons. 

^  Dr.  Chas.  S.  Bond  has  found  a  curved  aspirating  needle  with  lumen  about 
1  mm.  in  diameter  very  useful  in  tapping  the  pericardium  when  the  fluid  lies  back  or  is 
encapsulated.  The  needle  which  he  uses  has  a  radius  of  about  10  cm.  following  the  curve 
of  the  heart  and  enabling  him  to  pass  around  the  latter  without  injuring  it.  The  danger 
of  entering  the  ventricle  by  a  straight  push  is  also  much  less  with  an  instrument  of  this  form. 


496 


DISEASES   OF   THE    HEART    AND    AORTA. 


Sites  for  Paracentesis. — Trousseau  (1854)  recommended  introducing  the  needle  iti  the 
fourth  interspace  just  below  the  mammilla;  Dieulafoy  (1873)  in  the  fifth  about  six  centi- 
metres from  the  sternal  margin.  Puncture  at  these  sites  or  at  the  outer  border  of  absolute 
dulness  (flatness)  has  the  disadvantage  of  always  traversing  and  often  infecting  the  pleural 
cavity,  so  that  occasionally  the  patient  may  be  caused  gratuitous  empyema  or  even  a  fatal 
pneumonia. 

In  order  to  avoid  entering  the  pleural  cavity,  Baizeau  (1868)  and  Delorme  and  Mignon 
advocate  puncturing  the  pericardium  as  near  as  possible  to  the 
sternal  margin  in  the  fifth,  or  if  possible  the  sixth,  left  inter- 
space. In  order  to  render  the  procedure  more  certain,  the  latter  investigators  advise 
making  an  incision  through  the  skin  with  a  bistoury.  The  needle  (of  medium  diameter) 
is  then  introduced  into  the  sixth  interspace  if  possible,  and  otherwise  into  the  fifth  along 
the  edge  of  the  sternum,  pushed  in  for  a  centimetre  or  two,  and  then  the  point  directed 

downward  and  inward  by  a  slow  con- 
tinuous movement  until  the  liquid 
emerges.  In  order  to  empty  the  peri- 
cardial cavity  the  needle  should  be 
connected  with  an  aspirator  bottle  and 
the  fluid  collected  by  gentle  aspira- 
tion.' When  the  instrument  is  inserted 
slowly  in  the  manner  described,  the 
risk  of  injuring  the  heart  (right  ven- 
tricle) is  minimal,  for  the  beating  of 
the  latter  against  the  point  can  be  felt 
as  soon  as  it  is  touched  and  long 
before  it  can  be  penetrated.  Even 
if  through  lack  of  care  the 
right  ventricle  be  penetrated, 
harm  rarely  results.  For 
example,  Hulke  mentions  a  case  in 
which  he  penetrated  the  right  ventricle 
and  a  few  jets  of  blood  spurted  out, 
but  the  patient's  condition  improved! 
and  he  cites  several  other  similar  cases. 
Only  one  case  of  death  (from  laceration 
of  the  right  ventricle)  due  to  para- 
centesis is  on  record  (West).  Unques- 
tionably when  all  goes  well  the  technic  of  Delorme  and  Mignon  is  the  most  satisfactory, 
since  the  danger  of  injuring  both  heart  and  pleura  is  minimal.  On  the  other  hand,  the 
chance  of  a  "dry  puncture"  is  great.  At  the  place  selected  the  point  of  the  needle  may 
penetrate  a  great  deal  of  dense  fibrous  tissue  and  even  periosteum  and  the  lumen  may  thus 
become  plugged.  Should  the  fluid  not  appear,  this  source  of  error  may  be  obviated  by 
carefully  inserting  a  wire  through  the  whole  length  of  the  needle  after  it  has  been  pushed 
into  the  cavity  and  then  withdrawing  the  wire.  Another  difficulty  may  lie  in  the  position 
of  the  heart  itself,  as  occurred  in  the  above-mentioned  case  of  the  writer's,  in  which  the 
heart  instead  of  lying  behind  the  fluid  lay  directly  against  the  chest  wall  in  the  position 
described  by  SchaposchnikofT.  When  the  needle  was  introduced  by  Dr.  Cole,  it  encountered 
the  heart  at  once,  and  the  rubbing  of  the  latter  against  the  point  could  be  readily  felt. 
This  might  have  been  prophesied  from  the  fact  that  the  heart  sounds  were  well  heard  over 
the  precordium.  With  the  exception  of  a  few  cubic  centimetres  of  clear  fluid  the  puncture 
was  a  dry  one,  in  spite  of  several  successive  insertions  of  the  needle  both  at  this  point  and 
in  the  costoxiphoid  angle.  The  patient's  condition  became  very  bad,  and  he  died  before  a 
second  paracentesis  could  be  undertaken.  Autopsy  showed  the  heart  lying  directly  against 
the  chest  wall  with  1200  c.c.  of  fluid  above  and  to  the  left.  In  this  case,  as  in  all  those  in 
which  the  heart  sounds  and  pericardial  friction  are  well  heard  at  the  time  of  paracentesis, 


Fig.  285. — Sites  for  paracentesis  pericardii  and  peri- 
carditomy.  Ri,  Riolan  (1646),  trephining  the  sternum; 
D  &  M,  Delorme  and  Mignon  (1895),  paracentesis; 
li,  Romero  (1819),  pericardiotomy;  E,  v.  Ei.selsberg's 
pericardiotomy;  Tr,  Trousseau  (1854);  Di,  Dieulafoy 
(1873),  paracentesis;    W,  West,   pericardiotomy   (1883). 


*  Sewall,  J.  Am.  M.  Asso.,  Chicago,  1909,  advises  aspirating  the  fluid  into  the  aspirator 
bottle  by  sucking  out  the  air  with  the  mouth  instead  of  with  a  mechanical  aspirator.  The 
procedure  is  simpler  and  mistakes  and  failures  of  the  pump  are  impossible. 


PERICARDITIS.  497 

it  would  have  been  better  to  have  introduced  the  needle  at  the  outer  border  of  cardiac  flat- 
ness in  spite  of  puncturing  the  pleura,  and  to  have  risked  empyema  to  save  the  patient. 

Drainage  of  the  Pericardium. — Prof.  Pearson,  of  Cork,  punctures  the  pericardium, 
with  a  large  trocar,  withdraws,  and  then  introduces  a  fine  rubber 
catheter  into  the  pericardial  cavity  through  the  tube  of  the  trocar.  The  rubber  catheter 
follows  the  curves  of  the  pericardium  without  danger  of  rupturing  it,  and  thus  enables  him 
to  reach  exudates  which,  as  in  the  case  of  R.  C.  W.  B.  cited  above,  are  located  behind 
the  heart.  He  also  withdraws  the  metal  tube  and  leaves  the  rubber  tube  in  place  as  a 
permanent  drain  for  several  days  at  a  time,  and  states  that  in  this  way  he  has  been  able 
to  cure  a  number  of  stubborn  cases  of  chronic  pericarditis  with  effusion  which  had  resisted 
all  other  methods  of  treatment. 

The  fact  cannot  be  too  greatly  emphasized  that  cases  with  pericardial  effusion  are 
usually  desperate  cases,  and  the  fluid  should  be  gotten  out  at  all  hazards.  It  is  true  that 
all  the  fluid  need  not  be  removed  to  effect  recovery,  since  the  removal  of  a  small  amount, 
just  as  in  Starling's  experiment,  allows  the  circulation  to  re-establish  itself  and  often  per- 
mits the  rest  to  be  absorbed. 

Resection. — As  has  been  seen,  paracentesis  pericardii,  even  in  cases 
of  simple  serous  pericarditis,  may  be  far  from  satisfactory.  In  purulent 
pericarditis  and  hsemo-  and  pneumopericardium  it  is  still  less  so.  In  such 
cases  paracentesis  is  inadequate  and  the  pericardium  must  be  opened 
freely.  Radical  as  this  procedure  may  seem,  its  satisfactory  performance 
by  Romero  antedates  paracentesis.  Romero  made  an  incision  in  the  fifth 
intercostal  space  at  the  level  of  the  costochondral  articulation,  introduced 
his  finger  into  the  wound,  palpated  the  pericardium  with  his  finger,  and 
then  seized  it  with  forceps  and  opened  it  with  curved  scissors.  The  opera- 
tion is  best  performed  under  light  chloroform  anaesthesia.  Though  this 
must  be  carefully  administered  on  account  of  the  cardiac  weakness,  it  is  a 
significant  fact  that  most  of  the  patients  have  stood  the  anaesthetic  well. 

The  site  for  free  incision  has  varied  with  different  operators.  Rosen- 
stein  made  a  free  incision  in  the  fourth  left  interspace  close  to  the  sternum 
and  then  inserted  a  rubber-tube  drain.  West  operated  in  the  fifth  left 
interspace  in  the  nipple  line,  having  previously  introduced  an  aspirating 
needle,  which  he  used  as  director  for  a  long  narrow-bladed  sharp-pointed 
bistoury,  subsequently  enlarging  the  opening  with  a  probe-pointed  bistoury. 
V.  Eiselberg  resected  the  fourth  costal  cartilage  and  then  opened  the  peri- 
cardium. Delorme  and  Mignon  perform  what  is  probably  the  least  danger- 
ous and  most  satisfactory  operation.  They  disarticulate  the  fifth  and  sixth 
costal  cartilages  from  the  sternum  with  a  pointed  bistoury,  draw  them 
forward  one  by  one,  and  fracture  them  about  4  cm.  from  the  sternum. 
They  then  dissect  down  to  the  pericardium,  which  they  pull  forward  with 
forceps,  and  then  slit  it  up  with  scissors  for  several  centimetres.  , 

Many  observers,  from  Aran  to  the  present,  supplement  the  simple 
drainage  with  irrigation  of  the  pericardium.  Aran  injected 
a  dilute  tincture  of  iodine  at  100°,  a  procedure  which  in  his  case  (though  not 
in  all  others)  did  not  cause  pain;  West  used  warm  1  per  cent,  carbolic 
acid;  others  used  simple  salt  solution.  The  importance  of  irrigation  can- 
not be  too  freely  emphasized,  since  the  treatment  should  aim  not  only  at 
recovery  but  also  at  reducing  the  exudate  and  the  resulting  adhesions  to 
a  minimum. 

Delorme  and  Mignon  operated  upon  all  forms  of  pericardial  effusions. 
Their  conclusions  are  summed  up  in  the  following:     "  100  observations 

32 


498  DISEASES   OF   THE   HEART   AND    AORTA. 

— 82  paracentesis,  IS  incision:  82  paracentesis — mortality  65  per  cent.; 
18  incisions — mortality  38  per  cent.  Let  us  do  for  the  pericardium  what 
we  have  done  for  the  peritoneum." 

The  relative  merits  of  palliative  therapy,  paracentesis,  and  free  incision 
are  well  shown  in  West's  case  of  purulent  pericarditis : 

A  van  boy,  aged  16,  was  struck  in  the  back  by  a  truck  and  knocked  down.  No  sjTnp- 
toms  for  two  months,  then  shivering  and  pain  in  the  left  side  and  precordium.  Pain  sub- 
sided in  a  few  days.  Three  weeks  later  he  went  out  for  a  short  walk;  became  very  faint 
and  almost  fell  down.  Pain  seized  him  in  the  pit  of  the  stomach.  Became  cyanotic,  dys- 
pnoeic,  and  nauseated.  Admitted  Sept.  7.  Pulse  78;  paradoxic,  losing  2-3  beats  at  each 
inspiration.  Precordial  bulging  and  oedema.  Dulness  from  right  nipple  line  to  three  inches 
outside  left  nipple  line.  Cardiac  sounds  almost  inaudible.  Liver  pushed  down  and  felt  in 
epigastrium.     Slight  oedema  of  feet. 

Twelve  leeches  applied  to  the  precordium  followed  by  poul- 
tices.    Palliative  treatment  for  a  week.     Pulse  and  general  condition  feebler. 

Sept.  14.  Paracentesis  pericardi i — fourth  left  interspace  below  nipple ; 
90  CO.  1  per  cent,  carbolic  acid  at  100°  then  introduced  through  the  needle  and  used  to 
wash  out  pericardial  ca\'ity.     No  pain.     Patient  much  relieved. 

Sept.  17.  Patient's  condition  again  bad.  Paracentesis  fails  to  remove  fluid.  Free 
incision  under  chloroform,  as  above  described,  in  fifth  left  interspace;  at  least 
two   quarts   of   pus   removed.     Immediate  improvement.    Uneventful  recovery. 

Left  hospital  Feb.  23,  and  the  following  September  was  perfectly  well  and  had  been 
follo\\ang  his  usual  work  for  the  past  six  months  as  well  as  ever. 

Rosenstein's  case  and  those  of  Delorme  and  Mignon  show  .similar 
results. 

West  gives  the  following  statistics  for  paracentesis: 

Phthisis 

Rheumatic  fever 

Scurvy 

Pleurisy 

Injury 

Pneumonia 

General  dropsy: 

Morbus  cordis 

Nephritis 

Chronic  bronchitis 

Mediastinal  tumor  

Unassigned 

67  34  33 

In  spite  of  the  comparative  harmlessness  and  brilliant  results  obtained 
by  the  radical  operation  in  purulent  pericarditis,  it  is  not  probable  that 
this  procedure  can  be  extended  to  the  milder  exudates,  since,  just  as  in 
joints,  free  prolonged  drainage  is  followed  by  complete  obliteration  of  the 
cavity.  Irrigation  of  the  cavity  through  an  aspirating  needle  or  trocar, 
after  tapping,  is  possible  only  when  the  diameter  is  large  and  the  outflow 
is  a  free  one. 


Number. 

Recovery. 

Deat 

13 

4 

9 

11 

7 

4 

9 

6 

3 

6 

5 

1 

3 

2 

1 

2 

2 

2 

2 

2 

2 

1 

1 

1 

1 

17 

7 

10 

PERICARDITIS.  499 

BIBLIOGRAPHY. 
Pericakditis. 

Historical  data  are  taken  from  G.  A.  Gibson,  Diseases  of  the  Heart  and  Aorta,  Edinb.  and 

Lond.,  1898. 
Poynton,  F.  J.:  Heart  Disease  and  Thoracic  Aneurism,  Lond.,  1907. 
Sturges.     Quoted  from  McPhedran,  A.:  Pericarditis,  Osier's  Mod.  Med.,  Phila.,  1908,  iv. 
Cadet  de  Gassicourt.    Quoted  from  Hochsingers  in  Pfaundler  and  Schlossmann's  "Diseases 

of  Children,"  translated  by  Shaw  and  La  Fetra,  Phila.,  Lippincott,  1908. 
Sears.     Quoted  from  Osier,  Principles  and  Practice  of  Medicine,  4th  edition,  N.  Y.,  1901. 
Chatard,  J.  A.:  Acute  Pericarditis  complicating  Acute  Lobar  Pneumonia,  Johns  Hopkins 

Hosp.  Bull.,  Balto.,  1905,  xvi,  334. 
Breitung:  Ueber  pericarditis  tuberculosa,  Berl.,  1877. 
Head,  Henry:  On  Disturbances  of  Sensation,  with  Especial  Reference  to  the  Pain  of 

Visceral  Disease,  Brain,  Lond.,  1896,  xix,  153. 
Emerson,  C.  P.:  Bull.  Johns  Hopkins  Hosp. 

Silva.     Quoted  from  Buxbaum,  B.:  Lehrbuch  der  Hydrotherapie,  Leipz.,  1903. 
Rubino,  A.:  Les  pericarditis  exp^rimentales  et  bact^riques.  Arch.  Ital.  de  Biol.,  1892, 

xvii,  298,  and  Rif.  Med.,  1892,  viii. 
Romberg,  E.:  Lehrbuch  der  Krankheiten  des  Herzens  und  der  Blutgefasse,  Stuttgart, 

1906. 
Verney:  Gaz.  hebd.  de  m^d..  Par.,  1856,  iii,  793.     Quoted  from  Thayer,  W.  S.:  Observa- 
tions on  Two  Cases  of  Pericarditis  with  Effusion,  Bull.  Johns  Hopkins  Hosp.,  Balto., 

1904,  XV,  149. 
Frangois-Franck,  A.:  Recherches  sur  la  mode  de  production  des  troubles  circulataires 

dans  les  epanchements  abandons  du  pericard,  Gaz.  hebd.  de  med.,  Par.,  1877. 
Lagrolet:  De  la  compression  du  cceur  dans  les  epanchements  du  pericard.  These,  Paris, 

1878. 
Cohnheim,  J.:  Vorlesungen  ueber  allgemeine  Pathologie,  Berlin,  1882. 
Starling,  E.  H.:  Some  Points  in  the  Pathology  of  Heart  Disease,  Lancet,  Lond.,  1897,  i, 

569,  652,  723. 
Bolton,  C:  The  Experimental  Production  of  Uncomplicated  Heart  Disease,  with  Especial 

Reference  to  the  Pathology  of  Dropsy,  J.  Path,  and  Bacteriol.,  Edinb.  and  Lond., 

1904,  ix,  67. 
Auenbrugger,  L.,  and  Corvisart.    Quoted  from  Ebstein. 
Rotch,  T.  M. :  Absence  of  Resonance  in  the  Fifth  Right  Interspace  diagnostic  of  Pericardial 

Effusion,  Bost.  M.  and  S.  J.,  1878,  xcix,  389,  421. 
Ebstein,  W.:  Zur  Diagnose  der  Fliissigkeitsansammlung  im  Perikardium,  Virchow's  Arch., 

1893,  cxxx,  418. 
Aporti,  F.,  and  Figaroli,  P.:  Zur  Lage  der  akutentstandenen  Ergiisse  im  Herzbeutel, 

Zentralb.  f.  inn.  Med.,  1900,  xxi,  737;    from  whom  Concato,  Riv.  clin.  di  Bologna, 

Anno  vii,  Fasc.  4,  is  quoted.. 
Sibson:  Article  on  Pericarditis  in  Reynolds's  System  of  Medicine,  Lond.,  1877. 
Koranyi,  F.:  Ueber  den  Perkussionsschall  der  Wirbelsaule  und  dessen  diagnostische  Yer- 

wentung,  Ztschr.  f.  klin.  Med.,  Berl.,  1906,  Ix,  295. 
Thayer,  W.  S.:  Observations  on  Two  Cases  of  Tuberculous  Pericarditis  with  Effusion, 

Johns  Hopkins  Hosp.  Bull.,  Baltimore,  1904,  xv,  149. 
Pirogoff.     Quoted  from  Schaposchnikoff. 
Schaposchnikoff,  B.:  Zur  Frage  ueber  Perikarditis,  Mittheil.  a.  d.  Grenzgeb.  d.  Med.  u.  d 

Chir.,  Jena,  1897,  ii,  86. 
Riolan  and  Romero.    Quoted  from  Schaposchnikoff,  Delome  and  Mignon. 
Jowett.     Quoted  from  S.  West. 

Dieulafoy:  Traite  de  I'aspiration  des  liquides  morbides.  Par.,  1873. 
Delorme,  E.,  and  Mignon:  Sur  la  ponction  et  incision  du  pericarde,  Rev.  de  Chir.,  Par., 

1895,  XV,  797,  987.  and  1896,  xvi,  56. 
West,  S.:  A  Case  of  Purulent  Pericarditis  treated  by  Paracentesis  and  by  Free  Incision, 

with  Recovery,  Statistics  of  Paracentesis  pericardii,  Med.  Chir.  Trans.,  Lond.,  188.3, 

Ixvi,  235,- 


500 


DISEASES   OF   THE    HEART    AND    AORTA. 


ADHERENT   PERICARDIUM. 

(Adherent  pericardium, — adhesive  pericarditis,  synechise  pericardii, 
concretio  pericardii  cum  corde,  chronic  mediastinopericarditis.) 

Whenever  a  pericardial  exudate,  fibrinous  or  fluid,  is  absorbed  slowly 
a  certain  amount  of  organization  takes  place  in  it  and  adhesions  form  just 
as  after  pleurisy  or  peritonitis.  The  form  of  these  adhesions  varies  consid- 
erably, from  long  thin  strands  stretching  like  cords  across  the  pericardial 
cavity  to  short  bands  of  dense  fibrous  tissue,  or  even  to  a  firm  tissue  which 


LONG 


DENSE 


Fig.  280. — Specimen  showing  the  two  layers  of  pericardium  united  in  some  parts  by  long  strands 
and  in  others  by  short  bands  of  dense  adhesions.  (From  a  specimen  in  the  Army  Medical  Museum, 
Washington,  D.  C.) 


knits  the  two  surfaces  together  and  completely  obhterates  the  cavity.  All 
these  forms  may  be  present  in  different  areas  of  the  same  pericardium,  so 
that  the  process  need  not  be  considered  as  perfectly  homogeneous. 

Moreover,  not  only  the  adhesions  within  the  pericardium  but  particu- 
larly the  extrapericardial  adhesions  which  are  formed  simultaneously  on 
the  outer  surface,  are  of  clinical  importance,  since  it  is  the  latter  which 
form  the  tightest  lines  in  the  harness  and  determine  the  strain  upon  the 
heart.  As  shown  by  Manges'  case  cited  below,  complete  obliter- 
ation of  the  pericardial  cavity  may  cause  no  symptoms 
as  long  as  the  extrapericardial  adhesions  remain  unimportant. 


PERICARDITIS. 


501 


The  main  adhesions  do  not  always  occupy  the  same  position,  but  may 
be  divided  into  the  following  groups  (Fig.  288) : 

1.  Chondropericardial — fixing  the  heart  to  the  costal  cartilages  and  chest  wall  in  front. 

2.  Pleuropericardial — gluing  it  to  the  pleura?  and  fixing  the  edges  of  the  lungs. 

3.  Mediastinopericardial — fixing    its    posterior    surface    and    especially   harnessing 
the  auricles. 

4.  Phrenopericardial — fixing  it  to  the  diaphragm. 


f 

i 

it.- 

*l 

m 

19! 

HI- 

y 

% 


Fig.  287. — Sections  showing  adherent  pericardium.  (Photomicrographs  by  Dr.  C.  S.  Bond.) 
A.  Seen  with  low  power.  B.  Same  specimen  under  high  power.  C.  Another  specimen,  showing  the 
extreme  vascularity  of  pericardial  adhesions. 


Each  of  these  gives  rise  to  a  distinct  group  of  physical  signs;  and,  since 
these  may  occur  separately,  it  is  important  that  they  should  be  consid- 
ered so. 

PATHOLOGICAL    PHYSIOLOGY. 

The  mechanical  effects  upon  the  circulation  due  to  pericardial  adhesions 
may  be  twofold:  1,  the  work  of  the  ventricle  is  increased  by  the  tug  upon 
the  adhesions;  2,  the  filling  of  the  heart  may  be  hindered  by  strangulation 
of  the  vena  cava.  At  each  contraction  the  heart  must  not  only  drive  out 
the  blood,  but  must  pull  on  its  harness  of  adhesions.  The  additional  work 
which  it  thus  has  to  perform  depends  both  upon  the    tightness  of  the 


502 


DISEASES   OF   THE    HEART    AXD    AORTA. 


adhesions  and  upon  the  weight  or  rigidity  of  the  structures 
pulled.  The  latter  factor  depends  upon  the  position  of  the  adhesions, 
whether  it  is  the  ribs,  pleura,  mediastinum,  or  the  diaphragm  and  liver  that 
are  tugged  upon,  being  greatest  for  adhesions  to  the  ribs  and  diaphragm. 
3.  The  emptying  of  the  heart  and  the  flow  through  the  aorta  may,  as 
claimed  by  Kussmaul,  be  hindered  by  the  tugging  of  the  adhesions  upon 
the  arch  of  the  aorta.  This  can  readily  be  shown  experimentally  if  such 
traction  be  made  in  a  dog  whose  chest  has  been  opened.  The  pulse  may 
be  made  to  disappear  absolutely  in  spite  of  the  fact  that  the  heart  rate 
remains  unchanged  and  the  heart  dilates  from  overfilling;  enough  blood 
flows  in  from  the  vensB  cavae  to  dilate  the  heart. 


PLE.P. 


Fig.  288. — Anterior  and  posterior  pericardial  adhesions.  (Semi-schematic.)  A,  Anterior  adhe- 
siona  showing  the  stumps  of  adhesions  to  the  ribs.  B.  Mediastinal  adhesions,  showing  a  side  view  of  the 
heart.  PLE.  P.,  pleuro-pericardial  adhesions;  C.  P.,  costo-  (or  cnondro)-pericardial,  P.  P.,  phreno-peri- 
cardial,  M,  P.,  mediastino-pericardial  adhesions. 


When  this  additional  work  is  imposed  upon  a  heart  already  weak,  it 
may  succumb  to  the  strain,  and  death  may  occur  with  all  the  manifesta- 
tions of  broken  compensation.  The  importance  of  adherent  pericardium 
in  causing  death  from  heart  disease  is  shown  by  the  fact  that  it  was  present 
in  almost  all  the  cases  of  Sturges'  series. 

Usually,  however,  the  ventricles  gradually  recover  from  the  strain  and 
simply  undergo  a  gradual  work  hypertrophy  proportional  to  the  additional 
strain,  and  an  additional  amount  of  work  may  be  done  at  each  systole 
suflicient  to  balance  the  amount  required.  During  exercise,  emotion,  dis- 
ease, or  other  strains,  however,  not  only  the  work  of  the  heart  in  the  circu- 
lation is  increased,  but  with  the  increased  systolic  output  and  systolic 
excursion  of  the  walls  the  tug  upon  the  adhesions  is  increased  enormously, 
and  the  heart  is  thus  readily  overstrained.  The  heavy  beating  of  the  heart 
under  emotional  excitement  is  especially  likely  to  bring  this  about. 

Moreover,  the  process  of  hypertrophy  is  not  a  pure  one.  With  the 
fibrosis  of  the  pericardial  adhesions  outward,  the  process  of  fibrosis  also 


PERICARDITIS.  503 

extends  inward  into  the  somewhat  injured  myocardium,  and  this  process 
goes  on  progressively  with  each  moment  of  overstrain  until  the  myofibrosis 
cordis  is  advanced  and  the  heart  failure  complete. 

The  site  of  the  adhesions  determines  not  only  the  degree  but  the  char- 
acter of  the  heart  failure.  If  the  densest  adhesions  are  over  the  left  ven- 
tricle, the  effect  is  to  inhibit  the  action  of  the  latter  alone.  Nature  performs 
the  experiment  of  ^^'elch,  and  gives  rise  to  the  clinical  picture  of  broken 
pulmonary  compensation  with  dyspnoea,  cardiac  asthma,  or  pulmonary' 
oedema. 

If  the  chief  adhesions  are  over  the  right  ventricle,  on  the  other  hand, 
broken  systemic  compensation  sets  in  with  venous  stasis,  tricuspid  insuf- 
ficiency, enlargement  of  the  Uver,  and  collection  of  fluid  at  various  sites, 
but  particularly  in  the  peritoneal  cavity  (cf.  Pseudocirrhosis,  page  509). 

On  the  other  hand,  the  tugs  of  the  adhesions  on  auricles  and  ventricles 
may  act  as  mechanical  extrastimuli  and  produce  an  extrasystolic  arrhyth- 
mia, which  in  itself  hinders  the  circulation. 

SYMPTOMS. 

Since  the  actual  formation  of  the  adhesions  really  represents  the  sub- 
sidence of  the  acute  pericardial  process,  it  is  not  surprising  that  the  onset  of 
the  pathological  lesion  is  insidious,  and  indeed  may  coincide  with  the  sub- 
sidence rather  than  the  onset  of  symptoms.  This  is  well  illustrated  by  cases 
of  purulent  pericarditis  like  that  reported  by  Manges,  in  which  obUteration 
of  the  pericardial  cavity  accompanied  the  curve  of  the  heahng  of  the  incision. 
The  patient  was  free  from  symptoms,  and  a  year  later  was  working  as  a 
messenger  boy.  In  most  cases  the  process  continues  insidiously  during 
months  or  years  before  cardiac  symptoms  and  heart  failure  set  in,  during 
which  the  patient  may  be  apparently  well  or  may  suffer  only  upon  over- 
exertion, over-indulgence  in  venere  et  potu,  or  emotional  excitement. 
Sooner  or  later  the  pump  wears  out  and  symptoms  become  marked. 

The  symptoms  of  adherent  pericardium  are  mainly  those  of  chronic 
heart  failure — palpitation,  weakness,  etc.  Precordial  pain  localized  about 
the  apex  or  the  base  of  the  sternum  is  common  (65  per  cent.-70  per  cent, 
of  cases) .  As  stated  above,  the  other  symptoms  may  fall  into  the  category 
of  cardiac  dyspnoea  or  that  of  venous  stasis  and  dropsy,  dependent  upon 
whether  the  failure  of  compensation  is  in  the  pulmonary  or  systemic  circu- 
lation. In  the  former  case  there  are  attacks  of  coughing  and  acute  dyspnoea, 
sometimes  wdth  smothering  sensations.  The  latter  often  begins  insidiously 
with  weakness,  enlargement  of  the  liver  and  spleen,  swelling  of  the  abdomen 
(Pick's  pericarditic  pseudocirrhosis  of  the  liver,  or  pericarditic  polyse- 
rositis), and  swelHng  of  the  feet.  These  symptoms  may  also  set  in  more 
acutely  as  in  the  form  of  simple  heart  failure. 

Delirium  occasionally  occurs  with  adherent  pericardium,  perhaps  due 
to  disturbed  cerebral  circulation.  In  one  case  under  the  writer's  care  the 
patient  was  subject  to  hallucinations  of  vision  during  the  periods  when  his 
cardiac  condition  was  bad.  These  were  probably  due  to  congestion  of  the 
retinal  capillaries,  so  that  he  saw  lions  and  tigers  jumping  over  one  another 
at  the  foot  of  his  bed,  even  though  he  realized  it  was  a  physiological  hallu- 
cination. 


504  DISEASES   OF   THE   HEART   AND   AORTA. 


PHYSICAL    SIGNS. 

Corresponding  to  the  variations  in  the  site  of  adhesions,  the  physical 
signs  of  adherent  pericardium  are  both  multifarious  and  interesting.  The 
patients  are  often  pale  and  pasty,  the  haemoglobin  being  low  and  the  ca- 
pillaries rather  empty  of  blood.  Sometimes  the  opposite  holds  true,  and 
plethoric  cyanosis  prevails.  Inspection  of  the  veins  of  the  neck  may 
show  filling  of  the  latter  during  inspiration  (Kussmaul's 
sign),  accompanied  by  inspiratory  diminution  in  the  size  of 
the  pulse  or  even  omission  of  some  beats  during  inspiration  (pulsus 
paradoxus,  Kussmaul)  (see  page  506).  The  sounds  over  the  heart  during 
this  period  may  become  weaker,  but  usually  still  continue. 

The  so-called  Friedreich's  sign  (diastolic  collapse  of  the  vein),  now 
known  to  represent  merely  a  weak  positive  venous  pulse  (see  page  57), 
is  common  to  many  weak  hearts  and  has  no  diagnostic  or  prognostic  value. 

C.  M.  Cooper  has  recently  added  what  seems  to  be  a  valuable  accessory  sign  of  ad- 
herent pericardium.  He  determines  how  long  the  patient  can  hold  the  breath  in  inspira- 
tion, and,  five  minutes  later,  the  same  for  holding  the  breath  in  expiration.  In  normal 
.    ^.   .,     ,      insp.  =40-70     .  j.      ,    .       25     .  .^         j.      •     ,        ^ 

mdividuals _on  on  >  ^"  cardiac  lesion   ,  ^  »  ^^  persons    with   mediastinal  and   pen- 

exp.  — ^u  ^o  lo 

insp.  =  9 

cardial  adhesions    ;--  (paradoxical  ratio).     Patients  with  bronchial  asthma  also 

exp.  =25 

insp.  =  15-20 
showed  _       „      (paradoxical  ratio);    so  that  its  chief   value   is   as   confirmatory 

evidence.     The  presence  of  a  paradoxical  ratio  may  prove  very  useful  in  confirming,  and 
a  normol  ratio  in  excluding,  mediastinopericarditis. 

Broadbent's  Sign. — The  chest  usually  shows  marked  precordial  bulging, 
especially  in  children.  Walter  Broadbent  in  1895  called  attention  to  a 
"visible  retraction,  synchronous  with  the  cardiac 
systole,  of  the  left  back  in  the  region  of  the  eleventh 
and  twelfth  ribs,''  and  " in  less  degree  of  the  same  region  of  the 
right  back "  (Broadbent's  sign) .  Such  retractions  of  the  interspaces 
have  also  been  recognized  in  many  cases  of  cardiac  hypertrophy  by  the 
Broadbents  as  well  as  by  other  observers  (Tallant).  J.  H.  F.  Broadbent 
has  lately  (Heart  Diseases,  4th  edition)  stated  the  tacts  more  definitely 
and  more  accurately  in  the  following  words:  ''The  systolic  recession  of 
spaces  alone  is,  however,  not  a  trustworthy  indication,  as  it  may  be  due 
to  atmospheric  pressure,  especially  when  the  heart  is  much  hypertrophied. 
When  the  costal  cartilages  or  lower  end  of  the  sternum 
are  dragged  in,  there  can  be  little  doubt  as  to  the  diagnosis,  as  this  could 
not  be  effected  by  atmospheric  pressure."  This  sign  is  often  most  marked 
in  deep  inspiration  when  the  diaphragm  is  tense. 

Broadbent  also  states  that  systolic  retraction  over  the  apex  is  a  valuable 
sign,  but  only  when  the  impulse  is  forcible  on  palpation,  as  it  may  otherwise 
be  due  to  atmospheric  pressure  (over  the  right  ventricle;  cf.  page  91), 
This  is  certainly  true  in  many  cases,  but  in  the  writer's  experience  there 
are  frequent  exceptions  to  this  rule,  and  it  is  of  value  chiefly  as  a  cor- 
roborating sign. 

Percussion. — The  area  of  cardiac  dulness  is  usually  but  by  no  means 
always  enlarged,  owing  to  the  hypertrophy  which  usually  takes  place. 


PERICARDITIS. 


505 


though  fixation  of  the  lung  borders  may  cause  the  area  of  flatness  and  area 
of  dulness  on  the  left  to  almost  coincide.  The  characteristic  features  on 
percussion  are :  Absence  of  the  usual  change  in  the  left 
border  of  flatness  between  deep  inspiration  and  deep  expiration. 
This  movement  of  the  border  of  the  lungs,  which  is  normally  2-3  cm., 
may  be  reduced  to  less  than  1  cm.  or  may  absolutely  disappear.  The 
position  of  the  apex,  as  determined  by  palpation,  auscultation, 
and  percussion,  also  becomes  fixed,  and  may  not  change 
at  all  when  the  patient  turns  from  lying  on  his  right  side  to  lying 
on  his  left.  However,  both  these 
fixations  may  be  present  with 
simple  pleural  adhesions  and  no 
actual  involvement  of  the  peri- 
cardial cavity.  This  was  well 
exemplified  in  the  case  of  a 
little  girl  who  had  been  a  pa- 
tient in  the  Johns  Hopkins 
Hospital  several  times  during 
the  last  couple  of  years,  and 
who  presented  signs  interpreted 
as  adherent  pericardium.  At 
autopsy  the  pericardial  cavity 
was  free  from  inflammatory 
processes,  but  the  pleurae  were 
everj^where  bound  down  tightly 
around  it.  Practically  the  effects 
were  nearly  the  same  as  if  the 
pericardial  cavity  had  been  in- 
volved, Broadbent's  sign  and 
pulsus  paradoxus  being  present 
to  a  slight  degree.  Such  cases 
are,  however,  extremely  rare,  and  difficult  to  diagnose  when  they  occur. 

Palpation.  —  Sir  William  Broadbent  has  called  attention  to  the  im- 
portance of  an  exaggeration  of  the  diastolic  shock  or  rebound 
(accompanying  the  second  sound)  over  the  greater  part  of  the  pericardium 
as  characteristic  of  adherent  pericardium.  This  is  certainly  a  useful  aid 
especially  in  corroboration  of  other  signs,  but,  unless  the  distinctness  of 
the  shock  is  far  greater  than  would  be  warranted  by  the  loudness  of  the 
sound  at  the  base,  it  is  of  httle  value.  Nevertheless,  the  writer  recalls  a 
case  in  which  the  diagnosis  of  adherent  pericardium  (accompanying  a  well- 
defined  aneurism)  was  based  upon  this  sign  alone  and  was  verified  at 
autopsy.  Professor  Thayer  has  found  that  there  is  often  in  addition  a 
protodiastoHc  shock  accompanying  the  third  heart  sound,  which  may  be 
the  most  intense  shock  in  the  whole  cardiac  cycle.  Apparently  this  is 
distinctive  of  adherent  pericardium. 

Thrills,  especially  presystohc  in  time,  are  occasionally  felt,  probably 
owing  to  tugs  upon  strands  of  adhesions,  but  these  alone  are  not  typical. 

Auscultation.— Since  pericarditis  is  frequently  (34  per  cent,  of  Sears's 
cases)  accompanied  by  various  forms  of  valvular  disease,  the  presence  of 


Fig.  289. — Cardiac  outline  in  adherent  pericardium. 
The  broken  line  indicates  the  fixation  of  the  left  border 
of  the  heart  (apex)  and  of  the  left  border  of  cardiac 
flatness  (anterior  margin  of  the  left  lung).  The  small 
diagram  at  the  left  shows  the  relation  of  the  heart  sounds 
to  the  cardiac  cycle,  indicating  the  unusually  loud  third 
heart  sound.  BR  BR  indicate  areas  of  systolic  retrac- 
tion of  the  ribs,  xiphoid,  and  interspaces;  R  1,  2,  Riess' 
gastric  soimds  in  adherent  pericardium. 


506 


DISEASES   OF   THE   HEART    AND    AORTA. 


all  varieties  of  valvular  murmurs,  especially  of  mitral  origin,  is  not  sur- 
prising. A  presystolic  rumble,  probably  due  to  the  stretching  of  strands 
of  adhesions  by  the  contraction  of  the  auricle,  is  occasionally  heard  in 
cases  of  adherent  pericardium  in  which  aortic,  mitral,  and  tricuspid  valves 
are  normal.  Sewall  also  reports  several  cases  with  reduplication  of  the 
first  sound,  which  was  shown  at  autopsy  to  be  due  to  old  peripheral  adhe- 
sions. Professor  Thayer  finds  the  third  heart  sound  and  the  corresponding 
protodiastolic  shock  and  wave  very  distinct  in  adherent  pericardium. 
This  may  be  due  to  the  fact  that  they  are  more  easily  transmitted  to  the 
chest  wall,  or  perhaps  because  the  filling  of  the  heart  causes  sudden  stretch- 
ing of  the  adhesions. 


Resp. 

RlEGELS  R 

Phenomenon  '  ^ 
Ven. 

Carot. 


Pulsus 
Paradoxus'  ' 


JJ  ^^^^\J^y^f\J\..^.^Aj 


COSTOPERIC 


-AMediastino 
peric 


Fio.  290. — Inspiratory  and  expiratory  dropping  of  beats  (Riegel's  pulse  and  the  pulsus  paradoxus) 
in  adherent  pericardium,  showing  the  position  of  the  adhesions  which  bring  the  condition  about.  VEN., 
jugular  pulse;  CAROT.,  carotid  pulse;  ftSSP.,  respiration  (downstrokes  represent  inspiration;  upstrokes 
represent  expiration).  In  cases  with  Riegel's  phenomenon  (anterior  costo-pericardial  adhesions)  the 
conditions  are  as  shown  in  the  diagram  (upper  respiratory  tracing,  venous  pulse,  carotid  pulse);  those 
with  pulsus  paradoxus  correspond  to  the  conditions  shown  by  venous  pulse,  carotid  pulse,  and  lower 
respiratory  tracing. 

Riess*  Gastric  Sounds. — ^A  very  interesting  sign  was  described  by  Riess 
in  1879,  and,  since  it  has  been  verified  by  so  excellent  an  observer  as  Fran- 
^ois-Franck,  merits  attention.  On  listening  over  the  stomach  in  some 
cases  of  adherent  pericardium,  observers  have  been  able  to  hear  the  heart 
sounds  loud  and  metallic  in  quality.  These  sounds  are  not  much  influenced 
by  changes  of  position,  by  respiration,  nor  by  inflation  or  filling  of  the 
stomach.  They  are  probably  due  to  adhesions  to  the  diaphragm  only,  and 
hence,  as  originally  stated  by  Riess,  are  not  present  in  all  cases  of  adherent 
pericardium. 

Variations  in  the  Pulse. — The  pulse  in  adherent  pericardium  is  usually 
small  and  rapid,  generally  regular,  but  often  showing  an  extrasystolic 
irregularity  which  is  probably  due  to  tugs  upon  the  strands  of  adhesions. 

The  striking  and  characteristic  feature  is  the  marked  diminution  of 
the  pulse-wave  during  inspiration,  amounting  sometimes  to  the  dropping 
of  a  beat  during  that  phase.  This  was  first  noticed  by  Griesinger  in  1854 
in  a  case  in  which  autopsy  showed  strands  of  adhesions  about  the  arch  of 
the  aorta,  causing  kinks  and  stenosis  in  its  lumen  when  pulled  upon  by  the 
descent  of  the  diaphragm.     The  venae  cavse  were  also  caught  in  dense 


PERICARDITIS. 


507 


adhesions  which  strangulated  them  in  similar  manner  during  inspiration. 
Both  inflow  and  outflow  of  blood  were  therefore  hindered  in  that  phase, 
hence  the  diminution  of  the  pulse.  The  same  condition  was  studied  by 
Hoppe  and  later  by  Kussmaul  (1873),  since  whose  report  it  is  known  as 
the  pulsus  paradoxus.  It  is  not  entirely  pathognomonic  of  adhe- 
rent pericardium  or  even  of  pericarditis  in  general,  occurring  with  open 
ductus  arteriosus  Botalli  (Frangois-Franck,  see  page  450)  and  in  many 
normal  or  neurasthenic  individuals  (Reichmann),  though  in  these  the  dimi- 
nution does  not  amount  to  complete  dropping  of  beats  during  inspiration. 


ADHES- 


Fig.  291. — A.  Radiograph  of  a  case  of  adherent  pericardium.  (Kindness  of  Prof.  C.  M.  Cooper.) 
B.  Diagram  illustrating  the  condition  seen  in  A,  showing  the  pericardium  pulled  outward  to  the  right  and 
a  portion  of  the  diapliragm  pulled  upward  by  the  adhesions  (ADHES). 


The  occurrence  of  exactly  the  opposite  condition  of  the  pulse,  namely  diminution 
of  the  wave  and  impulse  during  expiration,  has  been  described  by  Riegel  in  cases 
in  which  autopsy  showed  pleuropericardial  adhesions  upon  the  anterior  surface  of  the 
heart.  Riegel  believes  that  the  relaxation  of  the  lung  during  expiration  pulls  the  heart 
upward  and  produces  a  fall  of  pressure  from  displacement  of  the  latter. 

Rosenbach  has  been  able  to  show  experimentally  that  when  the  heart  was  displaced 
V)y  an  inflated  rubber  bulb  the  vense  cavae  became  kinked  and  the  pulse  became  smaller 
and  blood-pressure  fell.  When  this  displacement  occurs  during  inspiration  from  downward 
traction,  a  pulsus  paradoxus  results;  when  it  occurs  during  expiration,  Riegel's  phenom- 
enon occurs. 

Apart  from  these  respiratory  variations  the  blood-pressure  shows  no 
special  features,  being  usually  low  in  uncomplicated  cases;  but  it  is  fre- 
quently normal  from  compensatory  vasoconstriction  and  increased  cardiac 
effort,  and  occasionally  high  in  the  nephritic  and  uremic  cases. 

X=ray  Examination.  —  The  demonstration  of  pericardial  adhesions 
by  means  of  the  Rontgen  rays  was  first  made  by  Moritz  Benedikt  in  1897. 
Some  question  was  thrown  upon  his  methods  by  the  criticism  of  F.  Moritz 
(1900),  showing  that  normal  shadows  along  the  edge  of  the  cardiac  and 
liver  shadows  may  simulate  adhesions.  These  objections  were  obviated 
by  Stuertz,  who  reported  five  cases  in  which  the  presence  of  adhesions  was 
demonstrated  not  only  by  suspicious  shadows  through  the  lungs  and  along 
the  edge  of  the  pericardium,  but  also  by  the  fact  that  the  margin  of  the 
pericardium  at  these  points  was  pulled  downward  or  outward  when  the 
structures  were  rendered  tense  in  inspiration.    Some  areas  were  also  shown 


508  DISEASES   OF   THE   HEART    AND    AORTA. 

to  be  quite  fixed  during  respiration.  Stuertz's  observations  have  been 
confirmed  by  Lehmann  and  Schmoll  and  by  Dr.  C.  M.  Cooper,  to  whom 
the  writer  is  indebted  for  the  X-ray  shown  in  Fig.  291. 

The  special  value  of  the  X-ray  examination  lies  in  the  fact  that  it 
reveals  the  mediastinal  and  diaphragmatic  adhesions  with  accuracy,  and, 
by  demonstrating  the  points  at  which  the  fixation  and  tension  are  greatest, 
points  out  the  path  for  operative  interference. 

Abdomen. — The  abdomen  is  often  negative,  but  enlargement  of  the 
liver  and  spleen  and  ascites  are  frequent,  as  has  been  shown  by  Weiss  in 
1876. 

Case  of  Adhekent  Pericardium. 

The  following  very  typical  case  was  under  the  writer's  care  in  the  City  and  County 
Hospital  of  San  Francisco.  (As  the  original  history  was  lost,  these  notes  are  taken  from 
the  article  of  Lehmann  and  Schmoll,  who  have  previously  published  the  case.) 

L.  A.,  engineer,  23  years  old,  entered  the  hospital  complaining  of  headache,  nausea, 
and  shortness  of  breath.  He  had  had  rheumatism  six  years  before  admission,  and  then  had 
pain  over  the  heart.  Since  then  he  had  had  two  attacks.  During  the  past  few  years  he 
has  been  subject  to  periods  of  heart  failure  with  dyspnoea,  during  which  he  is  frequently 
depressed  and  sometimes  even  maniacal. 

The  patient's  lips,  ears,  and  extremities  are  deeply  cyanotic.  The  pulse  is  irregular, 
with  numerous  extrasystoles,  many  of  them  ineffectual.  The  apex  impulse  (systolic  pro- 
trusion) is  visible  in  the  sixth  interspace  3  cm.  outside  the  mammillary  line,  beyond  which 
there  is  a  well-marked  systolic  retraction  of  the  interspaces  in  front  and  back.  There  is 
also  systolic  retraction  of  the  ribs  and  costal  margin  (Broadbent's  sign).  The  apex  is 
fixed  and  does  not  move  with  change  of  position,  but  the  area  of  flatness  changes  during 
respiration  (movement  of  the  lung  border).  There  is  well-marked  pulsation  over  the  right 
ventricle.  Dulness  extends  above  to  the  third  rib  and  3  cm.  to  the  right  of  the  right  para- 
sternal line.  A  loud  presystolic  rumble  and  a  loud  systolic  murmur  are  heard  over  the  apex. 
The  second  pulmonic  is  markedly  accentuated.  Both  sounds  are  heard  with  the  extra- 
systoles. 

The  lungs  are  clear  except  for  dulness  and  bronchovesicular  breathing  at  the  left 
base  behind. 

The  liver  is  greatly  enlarged  and  readily  palpable,  but  there  is  no  pulsation.  There 
is  some  oedema  of  the  feet. 

Clinical  diagnosis:  Left-sided  pleurisy,  adhesion  of  the  pericardium  with  the  pos- 
terior surface  of  the  heart,  mediastinum,  and  diaphragm,  mitral  stenosis  and  insufficiency. 

Examination  with  the  fluoroscope  showed  the  heart  to  be  dilated  to  right  and  left. 
There  was  a  marked  angular  protrusion  along  the  right  border  of  the  cardiac  shadow. 
In  this  region  the  outlines  of  the  shadow  are  less  sharply  defined  than  usual,  merging  into 
the  liver  and  vertebral  shadows.  The  diaphragm  is  equally  high  on  left  and  right,  moving 
less  on  the  latter. 

The  patient's  condition  did  not  improve  under  rest  and  digitalis.  He  often  had  in- 
tense precordial  pains.  On  one  occasion  he  was  subject  to  definite  hallucinations,  imagin- 
ing that  he  saw  lions,  tigers,  and  other  brightly  colored  wild  animals  springing  to  and  fro 
upon  the  floor  of  the  ward  and  over  his  bed,  though  he  was  at  the  time  otherwise  rational, 
and  even  realized  that  it  was  an  hallucination.  He  was  placed  in  a  solitary  cell  for  twenty- 
four  hours  at  his  own  request,  for  fear  of  doing  personal  violence  to  the  persons  about  him. 

His  condition  became  so  much  worse  that  cardiolysis  was  decided  upon  as  a  last 
resort  and  was  performed  by  Professor  Stillman.  The  ribs  were  resected  over  the  pre- 
cordium  and  the  pericardium  opened  in  exploration.  The  heart  was  everywhere  covered 
with  adhesions,  which  over  the  anterior  surface  of  the  heart  consisted  of  strands  about  an 
inch  long.  There  was  no  fibrinous  exudate  and  no  fluid.  The  patient  took  the  ether  badly 
and  became  extremely  cyanotic.  The  shock  of  the  operation  did  him  evident  harm,  for 
during  his  entire  sojourn  after  that  he  felt  even  worse  than  before.  The  wound  itself  caused 
him  no  trouble  and  healed  per  primum.  The  patient  left  the  hospital  three  weeks  after 
the  operation,  in  spite  of  advice. 


PERICARDITIS. 


509 


Pericarditic  Pseudocirrhosis  of  the  Liver  (Pick),  and  Polyserositis  from 
Adherent  Pericardium  (Cabot). — Hutinal  in  1895  described  a  form  of 
liver  cirrhosis  of  cardiac  origin  (cirrhose  cardiaque).  Friedel  Pick  (1896) 
in  Pribram's  clinic  called  attention  to  a  very  interesting  clinical  condition 
which  is  not  infrequently  encountered,  but  whose  nature  is  often  over- 
looked. This  is  seen  in  certain  cases  which  run  the  course  of  a  primary 
hepatic  cirrhosis,  beginning  with  asci- 
tes, enlargement  of  the  liver,  slight 
jaundice,  general  weakness  and 
dyspnoea,  but  devoid  of  any  special 
cardiac  features.  Occasionally  there 
were  also  enlargement  of  the  super- 
ficial veins  of  the  abdomen  and  oedema 
of  the  feet.  The  first  and  second 
cases  were  considered  clinically  to  be 
primary  cirrhosis  of  the  liver,  and  the 
discovery  of  adherent  pericardium  at 
autopsy  came  as  a  surprise.  In  his 
third  case  adherent  pericardium  was 
carefully  sought  for  and  found,  and 
the  diagnosis  was  correctly  made. 
Death  occurred  in  two  to  four  years 
after  onset  of  symptoms.  The  peri- 
cardia in  these   cases  were   found   to 

be  completely  or  almost  completely  adherent,  the  rest  of  the  heart  normal. 
The  livers  showed  both  interlobular  cirrhosis  and  chronic  perihepatitis 
(iced  liver,  Curschmann),  the  peritoneum  was  thickened,  and  chronic 
perisplenitis  was  present.  An  example  of  this  condition  is  found  in  the 
case  of  J.  M.  C.  cited  on  page  272,  in  whom  the  presence  of  adherent  pericar- 
dium was  not  suspected  during  life. 

In  1898  R.  C.  Cabot  described  a  similar  case.  Flesch  and  Schossberger  find  the  con- 
dition not  infrequent  in  children,  presenting  the  superficial  manifestations  of  a  primary 
cirrhosis  without  the^  presence  of  alcohol  and  syphilis  as  etiological  factors.  On  careful 
examination  the  presence  of  adherent  pericardium  is  readily  detected  by  its  usual  signs. 

Flesch  and  Schossberger  were  able  to  reproduce  the  condition  experimentally  in  dogs. 
They  produced  pericarditis  by  injections  of  tincture  of  iodine  into  the  pericardial  cavity 
and  allowed  the  animals  to  recover,  during  which  period  adherent  pericardium  occurred. 
After  a  few  months  ascites  and  oedema  set  in  and  the  animals  died.  Their  results  have 
been  confirmed  by  O.  Hess,  who  has  also  produced  cyanosis  and  cirrhosis  of  the  liver  by 
suturing  the  inferior  vena  cava  to  the  diaphragm. 

Another  point  in  the  differential  diagnosis  from  true  primary  cirrhosis  is  the  fact  that 
the  veins  of  the  arms  and  neck  are  usually  enlarged  to  almost  the  same  extent  as  those  of 
the  portal  system,  showing  that  the  stasis  is  not  confined  to  the  latter.  There  is  no 
caput  medusae. 


Fig.  292. — Case  of  pericarditic  pseudocir- 
rhosis. (After  Cabot.  Host.  M.  and  S.  J.,  1898, 
cxxxviii.) 


TREATMENT, 

The  treatment  of  adherent  pericardium  may  be  both  palliative  and 
operative.  The  palliative  treatment  is  simply  the  general  treatment  for 
cardiac  weakness:  rest,  diet,  and  cardiac  stimulants,  strychnine  and  digi- 
talis, during  the  onset  and  acute  stages;  careful  graduated  exercises  and 
training  during  the  period  of  relative  freedom  from  symptoms. 


510  DISEASES   OF   THE   HEART   AND    AORTA. 

It  is  impossible  to  remove  the  condition,  and  the  therapy  must  be 
simply  so  directed  that  that  which  cannot  be  cured  may  best  be  endured. 

Anaemia  should  be  treated  with  iron,  exposure  to  infection  avoided, 
and  general  hygienic  conditions  maintained.  For  reasons  mentioned  above, 
these  precuations  should  be  carried  out  even  more  carefully  than  for  simple 
valvular  disease. 

Surgical  Treatment  (Cardiolysis) .  —  In  1902  Brauer,  of  Heidelberg, 
introduced  a  simple  method  of  treatment  which  promises  to  revolutionize 
the  therapy  of  adherent  pericardium.  Brauer  proposed  ''to  relieve 
the  heart  functionally  by  breaking  the  strong  bony 
ring  of  ribs,  not  by  a  severe  operation  with  the  breaking  up  of  exten- 
sive adhesions  but  only  by  substituting  a  soft  covering  for  the  natural  bony 

covering  of  the  heart On  account  of  the  tremendous  strain  upon 

the  heart,  due  to  traction  on  the  chest  wall,  we  foresaw  a  danger  in  opera- 
tion under  narcosis The  operation  was  tried  upon  a  patient  with 

adherent  pericardium,  broken  compensation,  ascites,  and  oedema.  Seg- 
ments of  the  third,  fourth,  and  fifth  ribs  7  to  9  cm.  in  length  were  resected 
under  light  narcosis,  the  periosteum  being  carefully  removed.  The  patient 
made  an  uninterrupted  recovery.  His  pulse  soon  became  stronger  and 
more  regular,  the  ascites  and  oedema  disappeared,  and  he  was  able  to  do 
heavy   work  without  symptoms.     The  pulse  still  remained  irregular." 

Brauer  reported  two  other  cases  with  equally  good  results,  and  these 
have  been  confirmed  by  Beck,  Umber,  Meyer,  Westfeld,  Wenckebach, 
and  others.  Brauer  particularly  states  that  he  does  not  attempt  to  break 
up  the  adhesions,  as  Delorme  and  Carl  Beck  have  proposed,  since  he  believes 
that  this  operation  is  too  severe  and  that  the  adhesions  would  form  again 
too  rapidly,  although  he  states  that,  in  individual  cases,  this  might  be 
done  besides  his  operation. 

As  regards  the  indications  for  cardiolysis,  it  would  appear  that,  since 
the  adherent  pericardium  cannot  otherwise  be  relieved,  this  operation  is 
worthy  of  trial  whenever  symptoms  of  cardiac  weakness  occur  an^l  recur 
in  a  patient  with  well-marked  adhesions  to  the  chest  wall  (tugging  in  of 
the  lower  ribs,  fixation  of  the  left  border  of  flatness  on  inspiration,  immo- 
bility of  the  apex)  and  recur  in  spite  of  general  cardiac  hygiene.  It  is  not 
necessary  to  wait  for  the  complete  cardiac  break-down  to  prophesy  that 
this  must  sooner  or  later  occur  in  such  a  case,  and  to  see  that  the  sooner 
the  work  of  the  heart  is  relieved  the  longer  will  be  the  life  of  the  patient. 
Moreover,  it  is  evident  that  if  the  operation  is  performed  between  attacks 
of  cardiac  overstrain,  the  patient  is  in  better  condition  to  withstand  the 
shock  of  the  operation  and  the  danger  of  the  latter  is  diminished.  If  the 
cardiolysis  is  not  performed  until  the  patient's  heart  has  almost  completely 
given  way,  as  in  the  case  of  the  patient  with  the  visual  hallucinations 
referred  to  above,  he  can  scarcely  fail  to  suffer  from  the  shock  of  the  opera- 
tion; but  even  in  such  cases  Brauer's  results  have  been  striking,  and,  since 
there  is  no  other  mode  of  relief,  operation  is  warranted. 

It  must  be  confessed  that  in  such  cases  the  manner  in  which  the  anaes- 
thesia is  administered  determines  a  large  part  of  the  shock  from  the  opera- 
tion, and  may  prove  a  decisive  factor  in  the  outcome.  The  selection  of  the 
anaesthetist  constitutes  no  small  part  in  the  management  of  the  case. 


PERICARDITIS.  511 

The  question  also  arises  whether  operation  shoukl  be  advised  in  chil- 
dren or  adolescents  whose  pericardia  are  adherent  to  the  chest,  wall,  but  in 
whom,  owing  to  the  flexibility  of  the  latter,  the  symptoms  do  not  as  yet 
demand  operative  interference.  In  this  regard  each  case  must  of  course 
be  decided  upon  its  own  merits,  but  it  is  evident  that  as  age  advances  the 
rigidity  of  the  ribs  is  bound  to  increase  and  the  strain  upon  the  heart  pro- 
portionately. If  the  case  remains  relatively  free  from  symptoms  as  age 
advances,  it  should  be  left  alone;  but  if  the  progress  of  the  second  or  third 
decade  brings  with  it  increasing  cardiac  symptoms  or  the  signs  of  pericardi- 
tic  pseudocirrhosis,  the  question  of  early  cardiolysis  should  be  seriously 
considered.  Since  there  is  no  hope  that  children  will  "outgrow"  an  adhe- 
rent pericardium,  it  should  be  relieved  as  much  as  possible  before  the  strain 
has  ruined  the  heart  muscle.  When  valvular  lesions  are  present,  especially 
mitral  stenosis,  the  danger  from  operation  is  of  course  greater,  but  in  the 
hands  of  a  skilful  surgeon  this  is  much  less  than  might  be  expected  and  is 
probably  less  than  that  in  pericardiotomy  for  purulent  pericarditis. 

BIBLIOGRAPHY. 

Adherent    Pericardium. 

Manges,  M.:  Adherent  Pericardium,  Internat.  Clin.,  Phila.,  1905,  15  ser.,  i,  1. 

Hoppe,  F. :  Ueber  einen  Fall  von  Aussetzen  des  Radialpulses  wahrend  dpr  Inspiration  und 

die  Ursachen  des  Phanomens,  Deutsche  Klinik,  1854,  No.  3. 
Kussmaul:    Ueber   schwielige    Mediastino-pericarditis    und    paradoxen   Puis,   Berl.   klin. 

Wchnschr.,  1873,  x,  433,  445,  461. 
Friedreich,  N.:  Ueber  den  Venenpuls,  Deutsches  Arch.  f.  klin.  Med.,  Leipz.,  1865-6,  i,  241. 
Cooper,  C.  M.:  The  Respiratory  Ratio;    a  Preliminary  Note,  J.  Am.  M.  Assoc,  Chicago, 

1909,  lii,  1182. 
Broadbent,  Walter:  An  Unpublished  Physical  Sign,  Lancet,  Lond.,  1895,  ii,  200. 
Broadbent,  Wm.  H.:  Adherent  Pericardium,  Trans.  M.  Soc,  Lond.,  1897-8,  xxi,  109. 
Broadbent,  Wm.  H.  and  J.  H.  F.:  Heart  Disease  and  Aneurism  of  the  Aorta,  New  York, 

4th  ed.,  1906. 
Camac,  C.  N.  B.:  Broadbent's  Sign,  Johns  Hopkins  Hosp.  Bull.,  Balto.,  1898,  ix,  271. 
Tallant,  A.  W.:  Some  Observations  on  the  Occurrence  of  Broadbent's  Sign,  Boston  M. 

and  S.  J.,  1904,  cli,  457. 
Sewall,  H.:  On  a  Common  Form  of  Reduplication  of  the  First  Heart  Sound  due  to  Extra- 
cardiac  Causes,  Contrib.  Sci.  Med.,  Vaughan,  Ann  Arbor,  1903,  29. 
Riess,  L.:  Ueber  ein  neues  Symptom  der  Herzbutelverwachsung,  Berl.  klin.  Wchnschr., 

1878,  XV,  751.    Weitere  Beobachtungen  ueber  einer  die  Herztone  begleitende  Magen- 

consonanz  bei  Herzbeutelverwachsungen,  ibid.,  1S78,  xvi,  333. 
Frangois-Franck,   A.:  Des   bruits   extracardiaques   in   g^n^ral,   en   particulier  des   bruits 

gastrique  rhythmes  avec  le  coeur;    contribution  au  diagnostic  de  I'adh^rence  au  peri- 

carde,  Gaz.  hebd.  de  Med.,  Par.,  1885,  2  s^r.,  xxii,  757. 
Griesinger's  observation  (1854),  reported  by  A.  Widenmann,   Beitrag  zur  Diagnose  der 

Mediastinitis,  Diss.,  Tubingen,  1856. 
Hoppe,  F.:  Ueber  einen  Fall  von  Aussetzen  des  Radialpulses  wahrend   der  Inspiration, 

U.S.W.,  Deutsche  Klinik.  1854,  No.  3. 
Reichmann,  E.:  Die  inspiratorische  Verkleinerung  des  Pulses  (sogen  Pulsus  Paradoxus), 

Ztschr.  f.  klin.  Med.,  Berl.,  1904,  liii,  112. 
Riegel,  F.:  Ueber  extrapericardiale  Verwachsungen,  Berl.  klin.  Wchnschr.,  1877,  xiv,  657. 
Rosenbach,  O. :  Experimentelle  Untersuchungen  Ueber  die  Einwirkung  von  Raumbesch- 

rankungen  in  der  Pleurahohle  auf  den  Kreislauf  apparat.  Arch.  f.  path.  Anat.,  etc., 

Berl.,  cv,  215. 
Benedikt,  M.:  Wien.  med.  Wchnschr.,  1897. 
Moritz,  F.:  Miinchen  med.  Wchnschr.,  1900.    Quoted  from  Lehmann  and  Schmoll. 


512  DISEASES    OF   THE    HEART    AND    AORTA. 

Stuertz:  Zur  Diagnose  der  Pleuraadhiisionen  aus  Pericard  und  Zwerchfell,  Fortschr.  a.  d. 
Geb.  d.  Rontgenstr.,  Hamb.,  1904,  vii,  215. 

Lehmann  and  Schmoll:  Pericarditis  adliesiva  im  Rontgenogramm,  ibid.,  1905,  ix,  196. 

Cooper,  Charles  Miner:  Personal  communication. 

Pick,  F.:  Ueber  chronische  unter  dem  Bilde  der  Lebercirrhose  verlaufende  Pericarditis 
(pericarditische   Pseudolebercirrhose),   Ztschr.   f.   klin.  Med.,  Berl.,   1896,  xxix,  385. 

Cabot:  Bost.  M.  and  S.  J.,  1898. 

Flesch  and  Schossberger:  Diagnose  imd  Pathogenese  der  in  Kindesalter,  haufigsten  Form 
der  Concetio  Pericardii  cum  Corde,  Ztschr.  f.  klin.  Med.,  Berl.,  1906,  lix,  1.  Con- 
firmed also  by  Hess,  O.:  Diagnose  und  Pathogenese  der  im  Kindesalter  haufigsten 
Form  der  Concretio  Pericardii  cum  Corde,  Ztschr.  f.  klin.  Med.,  Berl.,  1906,  Ix,  174. 

Brauer,  L.:  Cardialyse,  Mimchen.  med.  Wchnschr.,  1902,  xlix,  982.  Untersuchungen  an 
Herzen  Cardiolysis  und  ihre  Indikationen,  Arch.  f.  klin.  Chir.,  Berl.,  1903,  Ixxi,  258. 

Beck.     Quoted  from  Brauer. 

Umber:  Perkiarditis  und  mediastinale  Verwachsungen  und  Cardiolysis,  Therap.  d.  Gegen- 
wart.,  1905. 

Wenckebach,  K.  F. :  Remarks  on  Some  Points  in  the  Pathology  and  Treatment  of  Adherent 
Pericardium,  Brit.  M.  J.,  Lond.,  1907,  i,  63.     Ueber  pathologische  Beziehungen  zwi- 
schen  Atmung  und  Kreislauf,  Samml.  klin.  Vortr  ,  Leipz.,  1907,  No.  465,  466. 
For  a  review  of  the  subject  see  also  Delatour,  H.  B.:  Surgery  of  the  Pericardium 

and  Heart.  Am.  J.  Surg.,  N.  York,  1909. 


XIII. 
WOUNDS  OF  THE  HEART  AND  CARDIAC  TRAUMA. 

Hippocrates  and  Celsus,  Paul  of  ^Egina,  Roland,  Lanfranc,  and  other 
writers  of  antiquity  taught  that  wounds  of  the  heart  were  followed  immedi- 
ately by  death;  but  Ambroise  Pare  (1552)  saw  a  gentleman  of  Turin  "who, 
although  wounded  in  the  heart  during  a  duel,  was  able  to  pursue  his  antag- 
onist 700  feet  before  he  dropped  to  the  ground  and  died."  Muler  (1641) 
treated  a  soldier  who  lived  for  fifteen  days  after  sustaining  a  wound  of  the 
heart, — an  observation  so  unheard  of  at  the  time  that  he  had  the  autopsy 
protocols  signed  by  the  commander  of  the  garrison!  Aprilis  (1680)  de- 
scribes a  wound  of  the  right  auricle,  after  receiving  which  the  man  had  lived 
for  five  days. 

The  results  of  modern  times  were  summed  up  by  G.  Fischer  in  1867 
(351  cases)  and  Loison  (1899)  (277  cases).  Fischer  found  the  wounds 
occurring  with  the  following  frequency: 

Death  within  a  few 

minutes.  Recovery. 

Right  ventricle 107 — 21 . 9  per  cent.              6 

Left  ventricle • .  •  95 — 25.  per  cent.              6 

Both  ventricles 24 — 34 .  per  cent.              2 

Right  auricle 28 — 25 .  per  cent. 

Left  auricle 13 — 38 .  per  cent. 

Apex 12                                          4 

Base 1                                          1 

Septum  ventriculorum 6                                          1 

Whole  heart 15 — 62 .  per  cent.              1 

Left  heart 5 

Right  heart 3                                        11 

Coronary  artery 1                                          1 

Pulmonary  artery 1 

Not  specified 40                                       17 

351  50  (11.2%) 

In  452  cases  there  were  50  (12  per  cent.)  of  spontaneous  recovery. 

EXPERIMENTAL    SURGERY. 

Elsberg  in  1899  made  a  verj^  careful  study  of  wounds  experimentally 
produced  in  the  rabbit's  heart.  He  found  that  those  produced  during 
systole,  when  the  heart  fibres  are  shortened,  become  enlarged  during  dias- 
tole and  hence  bleed  more  than  wounds  of  corresponding  size  produced 
during  the  latter  phase.  Wounds  that  completely  penetrate  the  heart  wall 
bleed  more  than  those  which  do  so  partially.  Those  which  enter  perpen- 
dicularly bleed  more  than  those  which  penetrate  obliquely,  for  in  the  latter 
case  the  walls  form  a  valve-like  approximation  during  systole.  Indeed 
Prof.  Barker  and  the  writer  have  produced  oblique  wounds  penetrating  the 
entire  wall  of  the  dog's  ventricle,  which  scarcely  bled  at  all. 

33  513 


514 


DISEASES   OF   THE   HEART    AND    AORTA. 


Even  the  smallest  incised  wounds  made  by  Elsbcrg  in  the  rabbit's 
auricle  were  always  fatal  unless  sutured,  while  those  of  the  right  ventricle 
were  more  fatal  than  those  of  the  left.  Wounds  of  2  mm.  or  less  in  the  left 
ventricle  frequently  healed  spontaneously.  However,  when  suture  was 
employed  a  large  part  of  the  ventricles  could  be  cut  through  and  the  ani- 
mal's life  saved. 

The  size  of  the  instrument  producing  the  injury  plays  little  role,  for, 
although  in  general  large  wounds  bleed  more  and  are  more  uniformly  fatal 
than  small  ones,  nevertheless  large  and  fatal  wounds  have  been  produced 
by  even  ordinary  needles.  For  example,  Thiemann  describes  the  case  of  a 
man  who  in  pressing  against  a  heavy  beam  accidentally  drove  a  sewing- 
needle  through  his  chest  wall,  where  it  became  imbedded  and  stuck  into  tlie 


Fig.  293. — Wounds  of  the  left  ventricle.  (From  specimens  in  the  Army  Medical  Museum,  Wasii- 
iugton,  D.  C.)  A.  Bullet  wound  in  the  heart  of  a  soldier  who  lived  for  two  days  after.  B.  Stab  wound  in 
the  left  ventricle  ;  death  within  two  hours. 


heart  wall,  ripping  one  hole  1.5  cm*  long  in  the  wall  of  the  right  auricle  and 
another  smaller  hole  in  the  wall  of  the  right  ventricle.  His  life  was  saved  by 
operation  four  and  one-half  hours  later. 

A  single  small  puncture  of  the  heart  wall  with  a  needle  with  prompt 
withdrawal  of  the  needle  and  no  laceration,  as  is  occasionally  done  in  para- 
centesis pericardii,  as  a  rule  causes  no  marked  disturbance  and  does  not 
require  operative  interference. 

Death  from  penetrating  wounds  of  the  heart  results  either  from  bleed- 
ing, or,  as  was  already  shown  by  Morgagni  and  by  Cohnhcim,  from  accumu- 
lation of  blood  within  the  pericardium  (see  page  487),  compressing  the 
auricles  and  preventing  the  entry  of  blood  into  the  heart. 

It  is  possible  that  in  the  rare  cases  of  instantaneous  death  the 
trauma  may  cause  the  ventricles  to  pass  into  a  state  of  fibrillation  and 
the  circulation  abruptly  cease.  There  is  no  proof  that  this  is  frequent, 
however,  and  the  cases  of  instantaneous  death  from  wounding  the  heart. 
are  less  common  than  might  be  expected. 


WOUNDS   OF   HEART   AND   CARDIAC  TRAUMA.  515 


SYMPTOMS. 

The  symptoms  accompanying  a  wound  in  the  thorax  which  suggest  a 
wound  of  the  heart  (intrapericardial  pressure)  are  those  of  angina  pec- 
toris—  pain  down  the  left  arm,  a  feeling  of  precordial  oppression  and 
precordial  pain,  especially  marked  on  expiration.  Pressure  upon  the  pre- 
cordium  increases  these  pains.  There  is  shortness  of  breath.  Occasionally 
there  are  abdominal  pain  and  spasm  of  the  abdominal  muscles  (Rehn).  As 
Fischer  pointed  out,  pain  is  also  felt  about  the  external  wound,  but  as  a 
rule  not  in  the  heart  itself.  Even  probing  of  the  heart  wound, 
while  it  may  give  rise  to  weakness  and  syncope,  is  not 
accompanied  by  pain.  Thus,  one  patient  whose  left  ventricle  had 
been  wounded  thought  that  the  knife  had  only  gone  through  his  clothes. 
Blood  is  often  found  spurting  from  the  wound  with  a  well-defined  pulsa- 
tion. Sometimes  it  is  foamy  and  mixed 'with  air,  indicating  that  the  lung 
has  been  penetrated. 

PHYSICAL    SIGNS. 

The  area  of  cardiac  dulness  is  increased  or  is  replaced  by  tympany 
(pneumo-ha3mopericardium).  The  heart  sounds  are  replaced  by  loud 
churning  or  water-wheel  murmurs.  The  blowing  murmur  caused 
by  the  jet  of  blood  passing  out  of  the  heart  may  also  be  distinguished. 

The  pulse  becomes  small,  weak,  rapid,  and  finally  imperceptible. 

Whenever  time  warrants,  an  X-ray  examination  should  be  done  at 
once,  and  the  bullet  or  foreign  body  located.  This  may  sometimes  be  very 
exactly  done  by  means  of  stereoscopic  pictures  and  greatly  simplifies  the 
operation. 

TREATMENT. 

Operative  interference  in  the  treatment  of  wounds  of  the  heart  was  first 
proposed  by  Rose,  who  confined  himself  to  opening  the  pericardium  and 
removing  the  blood  that  compressed  the  auricles.  This  procedure  was  often 
of  benefit  and  even  effected  cure  in  cases  where  bleeding  ceased  spontane- 
ously, but  when  the  heart  continued  to  bleed  it  was  of  no  avail. 

Up  to  this  time  it  had  been  thought,  in  spite  of  the  experiments  of 
physiologists,  that  suture  of  the  heart  wall  itself  would  be  accompanied  by 
instant  death.  But  in  1895  Salomoni  and  Del  Vecchio  demonstrated  that 
wounds  in  the  heart  of  the  dog  could  be  successfully  treated  in  this  manner; 
and  in  1896  Cappelen,  Farina,  and  Rehn  sutured  the  heart  wall  in  man. 
The  passing  of  the  sutures  had  no  ill  effects.  Cappelen's  and  Farina's 
patients  died  a  few  days  later  from  secondary  causes,  but  Rehn's  patient, 
who  had  received  a  stab  w^ound  in  the  right  ventricle,  operated  on  forty- 
eight  hours  after  the  injury,  recovered,  and  thus  a  revolution  in  cardiac 
surgery  was  made.  Rehn  had  demonstrated  that  wounds  of  the  heart 
could  and  should  be  successfully  explored  and  sutured  like  wounds  of 
other  viscera. 

If  the  patient  is  in  severe  collapse  from  loss  of  blood,  an  intravenous 
infusion  of  warm  salt  solution  (37°  C.)  should  be  begun  at  once  while  the 
operators  are  hastily  cleaning  and  disinfecting  the  field  of  operation.  As 
a  last  resort  a  direct  arteriovenous  transfusion  into  the  veins  of  the  arm 


516 


DISEASES   OF  THE   HEART   AND    AORTA. 


may  be  made  from  another  individual  by  the  method  of  Crile,  Buerger, 
or  Hartwell  while  the  operation  on  the  heart  is  going  on,  and  some  exsan- 
guinated patients  may  thus  be  saved. 

Operative  Procedure.  —  The  incision  should  be  sufficiently  large  to 
admit  of  a  satisfactory  exposure.  A  flap  is  made  in  the  chest  wall  over 
the  point  of  penetration,  usually  including  two  ribs  and  three  interspaces. 
The  flap  adopted  by  most  operators  is  horizontal  U  shaped  with  bifurca- 
tions pointing  to  either  left  or  right,  the  connecting  bar  passing  through 
either   sternochondral   or   costochondral   articulations.     Occasionally  the 


Fir,.  294. — Exposure  of  the  heart  for  .suturing  a,  wound.  (.A.fter  G.  T.  Vaughan,  J.  Am.  M.  Assoc., 
1909,  Hi.)  1,  heart;  2,  deep  sutures;  3,  superficial  sutures;  4  and  5,  retractors  on  the  pericardium;  C, 
left  pleural  line;  7,  flap  of  chest  wall  including  the  fourth,  fifth,  and  sixth  ribs;  8,  heart,  outlined  by 
broken  outline. 


form  is  that  of  an  upright  or  an  inverted  U,  a  H ,  or  an  H.  If  the  wound 
is  near  the  sternum  and  has  not  already  penetrated  the  pleura,  that  cavity 
should  not  be  opened,  and  the  cl  or  H  shaped  flap  is  the  best;  but  if  the 
wound  has  pierced  the  pleura,  any  convenient  exposure  may  be  adopted. 
The  incision  through  the  pectoralis  major  should  be  parallel  to  its  fibres 
which  may  be  retracted.  The  sternochondral  or  costochondral  articula- 
tions are  cut  through,  the  ends  of  the  incision  prolonged  along  parallel  to 
the  ribs,  and  the  flap  forcibly  reflected  back,  fracturing  the  costal  cartilages 
to  permit  a  wide  opening.  If  the  pleura  has  not  been  penetrated,  it 
should  be  pulled  toward  the  outer  edge  of  the  wound  with  retractors.  A 
free  incision  should  be  made  into  the  pericardium,  the  pericardial  cavity 
emptied  of  clots,  the  wound  in  the  heart  located,  and  sutured  with  a  fine 
curved  needle  and  silk  thread.    In  passing  the  sutures  the  heart  wall  may 


WOUNDS   OF   HEART   AND   CARDIAC  TRAUMA.  517 

be  grasped  with  forceps  without  danger,  the  irregularity  which  accom- 
panies the  passing  of  the  needle  representing  merely  a  few  extrasystoles 
resulting  from  the  irritation,  and  passing  off  rapidly.  Elsberg  never  ob- 
served sudden  stoppage  of  the  heart  and  fibrillation  following  the  inser- 
tion of  sutures.  The  writer,  after  several  hundred  experiments  upon  ex- 
posed dogs'  hearts,  is  able  to  confirm  these  statements  of  Elsberg.  Elsberg 
states  that  the  interrupted  suture  is  preferable  to  the  continuous,  for, 
though  it  takes  longer  to  apply,  it  injures  fewer  muscle  fibres  and  is  more 
certain  to  hold.  The  sutures  should  be  tied  during  diastole;  these 
do  not  tear  out  as  readily  as  sutures  tied  during  systole.  In  tightening  the 
sutures  the  two  serous  surfaces  of  the  wound  should  be  pushed  in  so  as  to 
be  brought  into  apposition.  The  surfaces  unite  by  the  usual  growth  of 
fibrous  tissue.  The  nuclei  of  the  muscle  cells  near  the  wound  seem  to  be 
increased  in  number,  and  there  is  some  amitotic  and  mitotic  division  but 
no  definite  regeneration  of  muscle. 

Control  of  Hemorrhage.  —  When  the  bleeding  was  so  profuse  that 
death  seemed  imminent,  Elsberg  found  it  necessary  to  adopt  provisional 
means  for  stopping  bleeding  while  putting  in  the  sutures.  For  this  he  used 
a  hastily  placed  tobacco-pouch  suture,  or  even  a  ligature  about  the  whole 
heart  just  above  the  wound.  (This  does  not  apply,  of  course,  to  wounds 
in  the  upper  half  of  the  ventricles.)  He  was  then  able  to  place  the  sutures 
bloodlessly,  after  which  the  provisional  ligature  was  removed.  In  this 
way  he  was  able  to  suture  tremendous  wounds  (2  cm.  in  a  rabbit's  heart, 
corresponding  to  about  10  cm.  in  the  human  heart),  with  66  per  cent, 
of  recoveries. 

Large  wounds  of  the  auricle  may  be  more  difficult  to  control.  Sauer- 
bruch  recommends  stopping  the  bleeding  by  gently  compressing  the  auricle 
between  the  middle  and  ring  fingers  while  grasping  the  point  to  be  sutured 
between  the  index  finger  and  thumb.  Rehn  finds  that  with  some  care  a 
ligature  may  be  placed  about  the  auricle  to  still  the  bleeding  while  the 
sutures  are  rapidly  put  in,  but  there  is  danger  of  death  from  fibrillation  if 
the  circulation  is  completely  cut  off.  The  writer  has  been  able  to  control 
the  hemorrhage  from  quite  large  wounds  in  the  dog's  heart  for  over  ten 
minutes  by  holding  his  finger  gently  against  the  wound.  The  heart's  action 
was  not  weakened  by  this  procedure,  nor  did  it  become  irregular;  and  suffi- 
cient time  was  gained  to  lay  the  sutures  carefully.  This  was  found  to  be 
more  bloodless,  and  for  large  wounds  more  convenient,  than  Elsberg's 
method  of  laying  temporary  sutures. 

If  possible  the  bullet  should  be  removed  unless  it  is  too  deeply  imbedded 
in  the  cavity  of  the  heart.  Under  these  circumstances  it  may  be  left  at 
least  for  a  subsequent  operation,  as  it  often  becomes  encapsulated  and  may 
do  no  further  harm.  All  operators  agree  that  operation  in  the  Sauerbruch 
negative  pressure  chamber  or  with  Brauer's  positive  pressure  lessens  the 
danger  of  pneumothorax,  and  is  therefore  advisable  when  it  requires  no 
delay.  It  is  particularly  useful  when  the  wound  is  about  to  be  closed,  to 
prevent  the  continuance  of  the  pneumothorax. 

As  regards  the  question  of  drainage,  each  individual  case  must  be  de- 
cided on  its  own  merits.  It  is,  of  course,  important  to  prevent  sepsis, 
purulent  pericarditis^  and  pyopneumothorax.     When  the  pleura  has  not 


518  DISEASES   OF  THE    HEART   AND    AORTA. 

been  pierced,  the  pericardium  may  be  closed  in  a  large  number  of  cases 
without  drainage  (Rehn's  statistics  show  4  cases — 3  cures,  1  death — with- 
out drainage  of  pericardium;  with  drainage,  5  cases — 5  deaths;  perhaps, 
however,  drainage  was  used  in  only  the  more  severe  cases).  When  the 
pleura  has  been  pierced,  it  should  usually  be  drained.  Whenever  bits  of 
cloth,  dirt,  etc.,  have  entered  the  wound,  it  should  always  be  drained. 

Before  closing  the  wound  the  pericardial  cavity  should  again  be 
explored  to  see  that  no  other  wounds  in  the  heart  wall  or  vessels  have 
been  overlooked. 

Occasionally  large  branches  of  the  coronarj^  arteries  are  found  to  be 
pierced  and  must  be  ligatured.  This  is  necessary,  and,  as  shown  by  Porter 
and  Baumgarten  (see  page  280),  is  not  always  fatal,  as  there  is  a  certain 
amount  of  collateral  circulation,  but  sudden  death  may  result  during 
subsequent  excitement,  so  that  in  such  cases  more  prolonged  rest  is  advisa- 
ble than  in  cases  of  simple  suture.  It  is  worthy  of  note,  however,  that 
this  complication  is  not  mentioned  in  the  twelve  cases  of  late  results  com- 
piled by  Rehn. 

After  closure  of  the  wound,  with  or  without  drainage,  administration 
of  urotropin  is  probably  advisable,  since  Crowe  has  found  that  it  is  excreted 
in  the  pleural  and  pericardial  fluids  in  a  concentration  sufficient  to  inhibit 
the  growth  of  bacteria;  and  Bernheim  believes  that  its  use  increases  the 
resistance  of  these  membranes  (in  dogs  at  least)  to  infection.  It  has, 
moreover,  no  harmful  effects. 

Results  of  Operation. — Since  Rehn's  first  operation  a  large  number  of 
cases  have  been  reported.  In  1907  he  was  able  to  collect  statistics  of  124 
cases — 49  recoveries  (39.5  per  cent.),  75  deaths  (60.5  per  cent.).  In  this 
series  there  were  only  15  cases  of  gunshot  wound,  but  in  a  series  of  30 
cases  of  the  latter  compiled  from  the  series  of  Ricketts,  Borchardt,  and 
Rehn,  there  were  14  recoveries  (46.6  per  cent.)  and  16  deaths  (53.4  per 
cent.).  Of  the  75  deaths  in  Rehn's  series  16  died  on  the  operating  table, 
17  died  of  loss  of  blood  and  collapse  within  two  days,  30  died  of  infection 
(purulent  pericarditis  and  empyema) .  In  many  cases  the  haste  of  operation 
prevented  disinfection  of  the  field.  One  patient  (Gerzen's)  died  of  sudden 
hemorrhage  on  the  fifty-third  day.  Rehn  also  collected  reports  of  1 2  cases 
from  nine  months  to  ten  and  one-half  years  after  operation.  In  nine  exam- 
ination of  the  heart  was  negative;  in  three  there  was  slight  dilatation. 
There  were  costopericardial  adhesions  in  5;  9  were  absolutely  free  from 
symptoms;  2  had  pains  down  left  arm;  1  precordial  pain.  Only  one  had 
symptoms  of  definite  cardiac  weakness. 

G.  T.  Vaughan  has  recently  summarized  and  tabulated  150  cases 
operated  on  between  1896  and  1909,  of  which  51  (34  per  cent.)  recovered, 
a  striking  contrast  to  the  12  per  cent,  of  recoveries  in  the  earlier  years  from 
which  Fischer's  series  was  taken. 


NON-PERFORATING   INJURIES. 

Injuries  of  the  chest  wall  which  do  not  enter  the  pericardium,  such  as 
blows  upon  the  chest,  frequently  produce  secondary  lesions  of  the  heart 
and  pericardium,  which  have  been  mentioned  in  previous  chapters. 


WOUNDS   OF    HEART   AND   CARDIAC   TRAUMA.  519 

The  first  case  of  cardiac  disease  from  contusion  was  recorded  by  Blan- 
card  in  1688  and  is  very  typical.  The  patient  was  a  peasant  45  years  of 
age,  previously  healthy,  who  was  run  over  by  a  hay-cart.  He  did  not 
sustain  any  fracture,  but  suffered  from  pain  in  the  chest,  dyspnoea,  then 
fever,  delirium,  and  died  11  days  later  of  purulent  pericarditis  and  myo- 
carditis. Similar  cases  were  recorded  by  Bonetus  (1700),  Akonside  (1766), 
and  numerous  other  writers  both  ancient  and  modern. 

Bernstein  in  1896  was  able  to  collect  126  cases  from  the  literature. 
In  autopsies  upon  42  of  these  cases  there  was  found 

Endocarditis  alone 16  times 

Myocarditis       "     0 

Pericarditis        "     10 

Endo-  and  myocarditis 4 

Peri-    and  myocarditis 5 

Endo-  and  pericarditis 5 

The  signs  and  symptoms  appeared : 

Immediately  after  the  trauma 67 . 6  per  cent. 

Within  one  month 17.5    "       " 

Within  one  year 4.7    "       " 

Later  than  one  year 7.1"       " 

Time  not  given 3.1    "       " 

G.  Fischer  gives  a  list  of  the  causes  of  traumatic  rupture  of  the  heart 
in  his  series: 

Run  over  by  or  crushed  between  wheels  of  wagon 21 

Crushed  by  machinery 4 

Falls  from  considerable  heights 13 

Falls  from  heights  of  10  feet  or  less 7 

Struck  by  falling  objects 6 

Kicked  in  chest 4 

Hurled  against  wall 2 

Kiilbs  has  recently  investigated  the  subject  experimentally.  The 
results  in  23  animals  within  12  days  of  the  injury  were: 

Hemorrhages  into  the  heart  valves 17  times 

(1  rupture  of  an  aortic  valve) 

Subendocardial  or  subpericardial  hemorrhages 10  times 

extensive  hemorrhage  into  the  septum 3  times 

Pericardial  hemorrhages 10  times 

Hemorrhages  from  lungs 6  times 

There  was  polymorphonuclear  infiltration  and  disintegration  of  muscle  fibres  in  the 
vicinity  of  the  hemorrhages. 

The  symptoms  and  signs  of  these  conditions  following  trauma  do 
not  differ  from  those  in  similar  lesions  due  to  other  causes,  and  have 
been  considered   under  those   heads. 


520  DISEASES    OF   THE    HEART    AND    AORTA. 

BIBLIOGRAPHY. 

Wounds  of  the  Heart  and  Cardiac   Trauma. 

For  historical  data  see — 
Ricketts,  B.  M.:  The  Surgery  of  the  Heart  and  Lungs,  New  York,  1904. 
Borchardt,  M.:  Ueber  Herzwunden  und  ihre  Behandlung.     Pfahlungs  verletzungen  von 

Herz  und  Lunge,  Samml.  khn.  Vortrage,  No.  411-412;    Chir.  No.  113-114,  Ser.  xiv, 

Heft  21-22,  Leipz.,  1906. 
Elsberg,  C.  A.:  An  Experimental  Investigation  of  the  Treatment  of  Wounds  of  the  Heart 

by  Means  of  Suture  of  the  Heart  Muscle,  J.  Exp.  Med.,  N.  Y.,  1899,  iv,  479. 
Fischer,  G.:  Die  Wunden  des  Herzens  und  des  Herzbeutels,  Arch.  f.  klin.  Chir.,  Berl., 

1868,  ix,  571. 
Loison,  E.:  Des  blessures  du  pericarde  et  du  cceur  et  de  leur  traitement,  Rev.  de  Chir., 

Paris,  1899,  xix,  49,  205,  774;    1899,  xx,  37. 
Rehn,  L.:  Zur  Chirurgie  des  Herzens  imd  des  Herzbeutels,  Arch.  f.  klin.  Chir.,  Berl.,  1907, 

Ixxxiii,  723. 
Rose:  Deutsch.  Ztschr.  f.  Chir.,  xx.     Rosenthal:.  Deutsch.  med.  Wchnschr.,  1895.     Del 

Vecchio:  Rif.  Med.,   1895;    Zentralbl.  f.  Chir.,   1895,  574.     Salomoni:    ibid.,   1896. 

Farina:  ibid.,  1896,  1224.     Quoted  from  Rehn. 
Rehn,   L.:  Ueber  penetrirende  Herzwunden  und  Herznaht,  Arch.  f.  klin.  Chir.,  Berl., 

1897,  Iv,  315. 
Buerger,  L.  A:  Modified  Crile  Transfusion  Cannula,  J.  Am.  M.  Asso.,  Chicago,  1908,  li,  1233. 
Hartwell,  J.  A. :  A  Simple  Method  of  Blood  Transfusion  without  Cannula,  ibid.,  1909,  Hi,  297. 
Thiemann:  Nadelstichverletzung  des  rechten  Herzventrikels  und  Vorhofs,  Arch.  f.  klin. 

Chir.,  Beri.,  1907,  Ixxxiii,  565. 
Sauerbruch,  E.  F.:  Die  Verwendbarkeit  des  Unterdruckverfahrens  bei  der  Herzchirurgie, 

ibid.,  1907,  Ixxxiii,  537;    also  The  Present  Status  of  Surgery  of  the  Thorax  and  the 

Value  of  the  Sauerbruch  Negative  Pressure  Procedure  in  the  Prevention  of  Pneumo- 
thorax, J.  Am.  M.  Asso.,  Chicago,  1908,  h,  808. 
For  discussion  of  the  positive  pressure  methods  see  Robinson,  S.:    Artificial  Intrapul- 

monary  Positive  Pressure;  Experimental  Applications  in  the  Surgery  of  the  Lungs, 

ibid.,  1908,  H,  803;  and  Green,  N.  W.,  and  Maury,  J.  W.  D.:  The  Positive  Pressure 

Method  of  Artificial  Respiration,  with  its  Experimental  Application  to  the  Surgerj'  of 

the  Thoracic  CEsophagus,  ibid.,  1908,  H,  805. 
Vaughan,  G.  T.:  Surgery  of  Wounds  of  the  Heart,   J.  Am.  M.   Asso.,  Chicago,    1909, 

lii,  429. 
Bernstein:  Ueber  die  durch  Kontusion  und  Erschiittenmg  entstandenen  krankheiten  des 

Herzens,  Ztschr.  f.  klin.  Med.,  Beri.,  1896,  xxix,  519. 
Klilbs:  Experimentelle  Untersuchungen  ueber  Herz  und  Trauma,  Verhandl.  d.  deutsch. 

path.  Gesellsch.,  Jena,  1908,  xii,  172. 


XIV. 
ANEURISM. 

Aneurism  (aneurysm)  (Gieek  avEvpia/ua  a  widening  out)  =  a  dilatation  of  artery  or 
veins  (Galen). 

An  aneurism  is  a  blood-containing  tumor  whose  walls  are  formed  by  the 
walls  'of  a  blood-vessel  and  whose  cavity  is  in  direct  connection  with  the 
blood-vessel  from  which  it  arises  (Osier). 

Historical. — Hippocrates  (430  B.  C.)  and  the  early  Greek  writers  do  not  seem  to  have 
been  familiar  with  aneurism,  but  its  occurrence  and  nature  were  well  known  to  Rufus  and 
Galen  (A.D.  131-201),  who  recognized  two  forms:  "one  from  dilatation,  the  other  from 
wounding  of  a  vessel,"  usually  from  venesection  followed  by  sepsis. 


Fig.  295. — Specimen  of  a  large  aneurism.     (After  Hotigli.) 

Vesalius  (1543)  was  the  first  to  recognize  aneurisms  within  the  thorax  and  abdomen 
and  was  even  able  to  make  the  diagnosis  of  thoracic  aneurism  during  life.  Ambroise  Pare 
(sixteenth  century)  recognized  the  existence  of  "aneurism  by  anastomosis,  rupture,  erosion, 
and  wound,  along  with  the  frequency  of  thrombosis  within  the  sack."  He  was  also  the  first 
to  suggest  that  venereal  disease  was  a  factor  in  the  genesis  of  aneurism.  The  role  of  syphilis 
was  demonstrated  definitely  by  Lancisi  (1728).  The  next  great  step  was  made  by  Scarpa 
(1805),  who  demonstrated  that  the  most  important  mechanical  factor  was  weakening  of  the 
middle  layer  of  the  arterial  wall,  a  fact  which  has  furnished  a  basis  for  the  more  modern 
pathology  of  aneurism. 

CL.\SSIFICATION  OF  ANEURISM. 

It  is  extremely  difficult  to  make  a  satisfactory  classification  of  aneu- 
risms, but  the  following,  which  is  based  upon  that  of  Osier,  may  suffice  for 

most  purposes: 

521 


522  DISEASES   OF  THE   HEART    AND    AORTA. 

1.  True  aneurism  (aneurysma  verum,  aneurysma  spontaneum),  in  which  one  or 
more  of  the  coats  of  the  artery  form  the  walls  of  the  tumor. 

A.  Dilatation    aneurism. 

(o)  Sacculated,  in  which  the  bulging  or  out-pocketing  of  the  walls  does  not 

embrace  the  whole  circumference  of  the  artery  and  is  sharply  localized. 
(6)  Fusiform  (or  cyhndroid)  aneurism,  in  which  the  dilatation  occurs  over  a 
larger  area  of  artery  whose  entire  circumference  is  involved  in  the  dilatation. 

2.  Dissecting  aneurism,  in  which  the  coats  of  the  artery  are  separated  and  a 
new  cavity  (sometimes  lined  with  endothelium)  is  formed  between  these  layers  (usually 
between  media  and  adventitia). 

3.  False  aneurism,  following  wound  or  rupture  of  an  artery,  consisting  of  a  peri- 
arterial haematoma,  all  the  coats  of  the  artery  having  been  penetrated. 

4.  Cirsoid  aneurism  or  telangioma,  a  tumor  consisting  of  a  large  number  of 
tortuous  arteries  which  are  continuous  with  the  artery  from  which  they  arise. 

5.  Arteriovenous  aneurism,  a  communication  between  artery  and  vein,  either 
direct,  aneurismal  varix,  or  with  the  intervention  of  a  sac,  varicose  aneurism. 

ARTERIES    AFFECTED. 

By  far  the  most  common  forms  are  the  true  aneurisms,  fusiform  and 
sacculated.  The  relative  frequency  in  the  various  arteries  is  shown  in  the 
following  statistics  of  530  cases  (Crisp) : 

Thoracic  aorta 175 

Pophteal  artery 137 

Femoral  artery 66 

Abdominal  aorta 59 

Carotid  artery 25 

Subclavian  artery 23 

Axillary  artery 18 

External  iliac  artery 9 

Cerebral  artery 7 

Common  iliac  artery 2 

Posterior  tibial  artery 2 

Gluteal  artery 2 

Pulmonary  artery 2 

Brachial  artery 1 

Subscapular  artery 1 

Ophthalmic  artery 1 

OCCURRENCE. 

According  to  a  large  set  of  statistics  compiled  by  Richter  and  by  Arn- 
spcrger,  aneurism  of  the  aorta  represents  one  of  the  not  infrequent  causes 
of  death,  0.6  per  cent,  of  total  mortality  (Emmerich),  Brodier  1.2  per  cent., 
Miiller  1.49  per  cent.;  in  American  cities  0.6  per  cent.,  Philadelphia  0.6  per 
cent.,  St.  Louis  0.2  per  cent. 

According  to  Gibbons  and  Richter  the  percentage  of  deaths  from  aneurism  in  San 
Francisco  from  1866  to  1870  (1.35  per  cent.)  was  much  greater  than  elsewhere  in  the 
United  States.  Dr.  Gibbons  has  informed  the  writer  that  aneurism  at  that  time  was  par- 
ticularly common  among  stevedores,  who  formed  a  considerable  percentage  of  the  popula- 
tion, and  in  whom  syphilis,  alcohol,  and  hard  work  were  ever-present  factors.  With  the 
passing  of  the  adventurer  and  the  stevedore  as  important  elements  in  the  population,  the 
percentage  of  aneurism  in  San  Francisco  has  diminished,  being  0.90  per  cent,  in  1880-1884, 
0.42  per  cent,  in  1890-1894,  0.33  per  cent,  in  1900-1904  (Gibbons). 

On  the  other  hand,  in  communities  where  syphilis  is  common  the  fre- 
quency of  aneurism  increases.  Thus,  it  is  eleven  times  more  common  in  the 
British  Army  in  India  than  in  the  civilians  at  home,  and  much  more  common 


ANEURISM.  523 

in  the  British  than  in  the  Austrian  and  German  armies,  where  venereal  dis- 
•ease  is  five  times  less  prevalent. 

Aortic  aneurism  is  much  more  common  in  men  than  in  women. 

Crisp 67  women  out  of  551  cases 

Agnew 26  women  out  of  269  cases 

Lisfranc 13  women  out  of  154  cases 

Richter 58  women  out  of  736  cases 


164  women  out  of  1810  cases 
9.05  per  cent.,  or  1  in  11. 

On  the  other  hand,  48  per  cent,  of  cases  of  carotid  aneurism  and  66  per 
oent.  of  dissecting  aneurisms  occurred  in  women. 

As  regards  age  Crisp's  cases  were  distributed  as  follows: 

1  to  10   1         50  to  60   65 

10  to  20   71         60  to  70   25 

20  to  30   51         70  to  80   8 

30  to  40   198         80  to  90   2 

40  to  50  129         90  to  101 1 

59  per  cent,  between  the  ages  of  thirty  and  fifty. 

As  regards  site  Lawson  gives  the  following  figures : 

Ascending  aorta 34 .     per  cent. 

Arch  of  aorta 34 . 8  per  cent. 

Descending  aorta 17.4  per  cent. 

Abdominal  aorta 13 . 8  per  cent. 

Hare  and  Holder  find  in  953  cases  collected  indiscriminately: 

Ascending 570  =  60 .     per  cent. 

Transverse  arch 104  =  10.6  per  cent. 

Descending 110  =11. 5  per  cent. 

Unclassified 169  =  17.5  per  cent. 

figures  which  are  certainly  unusually  high  for  the  ascending  portion. 

Aneurisms  are  by  no  means  always  single,  but  may  sometimes  be  mul- 
tiple. Two,  three,  "  or  even  a  score  "  may  appear  along  the  course  of  the 
aorta,  or  numerous  aneurisms  may  be  present  in  the  peripheral  arteries. 
The  condition  is  simply  the  manifestation  of  the  generalized  action  of  the 
factors  of  sclerosis  and  blood-pressure  on  the  arterial  walls,  and  multiple 
aneurism  formation  is  one  of  the  features  of  experimental  adrenalin 
aortitis  (Erb,  Jr.). 

The  symptoms,  signs,  and  diagnosis  present  no  specific  features,  except 
the  ease  with  which  the  other  aneurisms  may  be  overlooked  after  one  is 
diagnosed.  Careful  examination  and  especially  fluoroscopic  examination 
will  prevent  this  error. 

PATHOLOGICAL  ANATOMY  AND  PATHOGENESIS. 

No  change  of  pressure  that  can  occur  during  life  is  sufficient  to  dilate 
an  artery  to  the  proportions  of  even  the  smallest  aneurism.  According  to 
the  elasticity  curve  of  Roy,  the  dilatation  occurring  between  the  blood- 
pressure  of  120  and  170  mm.  Hg  is  about  20  per  cent,  of  the  diameter  of  the 
artery,  and  the  results  of  Grehant  and  Quinquaud  show  that  very  little  fur- 
ther dilatation  occurs  if  pressure  is  raised  until  the  arterj^^  ruptures  (at  a  pres- 
sure of  1680  to  4630  mm.  Hg;  10  to  20  times  the  blood-pressure  during  life). 


524 


DISEASES   OF   THE   HEART   AND    AORTA. 


Fig.  296. — Aneurism  arising  just  above  a  sinus 
of  Valsalva.  (From  a  specimen  in  the  Army  Medi- 
cal Museum, Washington,  D.  C.)  OR.,  orifice  throui^h 
which  the  aneurism  is  connected  with  the  aorta; 
AN.,  aneurismal  sac. 


Fio.  297. — Aneurism  of  the  ascending  arch  and 
innominate  artery.  (From  a  specimen  in  the  Army 
Medical  Museum.) 


D.  AOR. 


Fig.  298. — Aneurism  of  the  transverse  portion 
of  the  aortic  arch  penetrating  through  the  sternum. 
(From  a  specimen  in  the  Army  Medical  Museum.) 
JNNOM.,  innominate  artery;  L.  CAR.,  left  carotid 
artery;  L.  SUB.,  left  sublavian  artery;  D.  AOR., 
descending  aorta. 


Fig.  299. — Aneurism  of  thedescending aorta  eroding 
the  vertebrae.    The  sac  contains  a  laminated  clot. 


ANEURISM. 


525 


Changes  in  Arterial  Wall  in  Aneurism. — On  the  other  hand,  as  was 
first  shown  by  Scarpa  (1805),  aneurismal  dilatation  is  always  preceded  by 
changes  in  the  arterial  coats  and  especially  by  weakening  of  the  media. 
In  1875  Koester  showed  that  this  was  due  to  localized  degeneration  of  the 
elastic  fibres  as  the  result  of  certain  inflammatory  changes  in  the  vasa 
vasorum  of  the  media.  ''The  inflammatory  process  begins  in  the  vasa 
vasorum  on  the  exterior  of  the  blood-vessel,  follows  them  perpendicularly 
into  the  muscularis  (media) ,  and  distributes  itself  within  this  layer,  being 
most  intense  at  the  places  where  the  vasa  vasorum  break  up  into  capillaries. 
As  a  result  of  this  chronic  multilocular  mesarteritis,  the  media  (muscle 
fibres  and  elastic  fibres)  degenerate.  The  intima  (which  may  be  thickened) 
and  the  adventitia  unite  to  form  a  thick  and  very  vascular  membrane 
which  forms  the  wall  of  the  aneurism."  Since  these  studies  of  Koester, 
waiters  are  practically  agreed  that  the  degeneration  of  elastic  tissue  result- 
ing from  mesarteritis  is  the  underlying  cause  of  aneurism  formation. 


ELAS 


WALL 


Fig.  300. — Sections  through  the  wall  of  an  aneurism.  (Photomicrographs  made  by  Dr.  C.  S.  Bond.) 
A.  Section  through  the  wall  of  an  aneurism  showing  the  clot  unorganized.  B.  Orcein  stain  showing  the 
destruction  of  elastic  tissue  in  the  aneurism  wall.     Elastic  tissue  (ELAS)  stained  dark. 


Simple  arteriosclerosis  in  which  thickening  of  the  intima  is  the  essential 
feature  does  not  weaken  the  wall  of  the  artery  and  plays  no  role  unless  the 
media  be  destroyed.  This  fact  is  further  borne  out  by  the  experimental 
changes  in  the  artery  produced  by  injection  of  adrenalin  (see  page  257). 
The  resulting  lesion  is  a  mesarteritis  without  changes  in  the  intima,  quite 
dissimilar  to  the  ordinary  arteriosclerosis  of  man;  but  aneurisms,  and  even 
multiple  aneurisms,  are  present  in  a  large  percentage  of  the  animals.  Other 
toxic  substances,  bacterial  toxins,  lead,  alcohol,  nicotin,  lactic  and  other 
acids,  etc.,  produce  these  changes. 

Fabris  has  also  produced  aneurisms  by  external  cauterization  of  the 
arterial  wall  with  silver  nitrate.  A  local  inflammation  was  thus  set  up  in 
the  adventitia  and  media,  which  resulted  in  degeneration  of  the  fibres  of 
the  latter  and  their  replacement  with  young  fibrous  tissue  devoid  of  elastic 


526  DISEASES   OF   THE    HEART    AND    AORTA. 

fibres.  In  a  few  cases  there  was  slight  intimal  thickening.  The  resistance 
of  such  a  fibrous  tube  is  less  than  that  of  an  elastic  tube,  and  aneurismal 
dilatation,  sometimes  localized,  sometimes  fusiform,  took  place  in  from 
20  to  25  days. 

Etiological  Factors. — In  man  the  etiological  factors  of  aneurism  are 
those  that  produce  mesarteritis.  Chief  among  these  is  syphilis,  which,  as 
first  noted  by  Ambroise  Pare  and  Lancisi,  is  concerned  in  a  very  large  per- 
centage of  the  cases  (Klemperer  25  per  cent.,  Fraenkel  36  per  cent.,  Puppe 
36  per  cent..  Trier  40.5  per  cent.,  Heiberg  41.87  per  cent.,  Bramwell  50  per 
cent.,  Thieberge  50  per  cent.,  v.  Xoorden  54  per  cent.,  Gerhardt  56  per  cent., 
Schutz  64.7  per  cent.,  Welch  66  per  cent.,  Etienne  69  per  cent.,  Malmsen 
80  per  cent.,  Hanpeln  82  per  cent.,  Backhaus  85  per  cent..  Heller  85  per 
cent.,  Rasch  92  per  cent.).  This  is  especially  true  of  aneurisms  occurring 
in  young  men  and  women,  when  the  other  factors  of  arteritis  play  a  rela- 
tively less  marked  role  than  in  later  life;  so  that,  as  stated  by  Professor 
Osier,  the  presence  of  an  aneurism  in  a  man  or  woman  under  thirty  is 
almost  to  be  regarded  as  presumptive  evidence  of  syphilis.  Moreover, 
syphilitic  aortitis  is  often  most  intense  in  the  first  part  of  the  ascending 
aorta,  hence  the  commonness  of  the  lesion  at  this  site  (Heller).  It  must 
be  added,  however,  that,  though  the  careful  researches  of  Ophiils  have 
failed  to  substantiate  this  general  belief,  a  positive  Wassermann  reaction 
is  usually  obtained  in  such  cases. 

Other  factors  are  alcohol,  hard  work,  lead  poisoning,  tobacco,  gout, 
nephritis,  and  especially  the  infectious  diseases.  Trauma  (blows,  gunshot 
and  knife  wounds,  etc.)  furnishes  a  frequent  cause  for  aneurisms  of  the 
peripheral  arteries  and  abdominal  aorta,  but  is  much  rarer  in  thoracic 
aneurisms.  Cases  like  that  described  by  Hirsh  and  Robins  show,  however, 
that  it  is  a  factor  to  be  reckoned  with.  The  relative  importance  of  these 
factors  is  shown  by  the  figures  of  Etienne,  who  found  syphilis  as  a  cause 
of  166  out  of  230  aneurisms,  while  alcohohsm  was  present  in  only  28.  More- 
over, according  to  Hamilton,  aneurisms  are  extremely  rare  in  sanitaria 
for  alcoholics.  They  are,  however,  most  important  contributory  causes, 
not  only  increasing  the  arteriosclerosis  but,  by  raising  the  blood-pressure, 
increasing  the  liability  to  dilatation.  Thus,  aneurisms,  according  to  most 
writers,  are  particularlj^  common  in  syphilitics  who  perform  hard  work. 
This  is  exquisitely  shown  in  the  colored  patients  at  the  Johns  Hopkins 
Hospital,  in  whom  syphilis  is  very  common  and  who,  as  a  rule,  perform 
hard  work.  Among  these  persons  aneurisms  are  between  five  and  ten  times 
as  common  as  in  the  patients  in  the  white  wards  of  the  same  hospital.  The 
sudden  rise  of  blood-pressure  which  occurs  during  lifting  and  heavy  strains 
(cf.  page  132)  is  a  particularly  important  predisposing  factor,  and  the 
patient  often  notices  that  his  first  symptoms  occurred  at  the  time  of  a 
heavy  muscular  strain  or  began  ju.st  afterwards. 

EMBOLIC  AND  MYCOTIC  ANEURISMS. 

A  somewhat  rarer  form  of  aneurism,  described  by  Tufnell  (1853),  Ogle 
(1866),  Church  (1870),  Smith  (1870),  Ponfick  (1873),  and  Weinberger 
(1907),  is  the  so-called  embolic  or  mycotic  aneurism,  which  arises  especially 


ANEURISM.  527 

during  the  course  of  acute  septicaemias,  of  puerperal,  arthritic,  and  influen- 
zal origin.  Septic  emboli  become  lodged  astride  of  the  bifurcation  of  the 
smaller  arteries,  causing  necrosis  of  the  neighboring  portions  of  the  arterial 
wall,  which  may  protrude  or  form  a  true  aneurism,  or  may  rupture  into 
the  surrounding  tissues,  forming  a  false  aneurism.  These  arise  acutely 
during  the  course  of  the  febrile  diseases.  They  are  usually  multiple  and 
are  confined  to  the  smaller  arteries,  while  the  sclerotic  aneurisms  are  more 
common  in  the  larger  arteries. 


DEVELOPMENT    OF    THE    ANEURISM. 

Once  formed,  the  aneurismal  sac  expands  progressively,  usually  pushed 
outward  from  the  artery  along  the  lines  of  the  least  resistance  until  it 
meets  with  some  obstruction.  The  higher  the  blood-pressure  the  more 
rapid  is  the  dilatation.  When  pointing  freely  into  the  thoracic  cavity,  it 
may  expand  until  it  fills  almost  the  entire  half  of  the  cavity  before  ruptur- 
ing. On  the  other  hand,  if  the  proliferation  of  connective  tissue  in  the  wall 
of  the  aneurism  does  not  keep  pace  with  its  growth,  or  if  local  necrosis 
from  infection,  pressure,  or  irritation  takes  place,  a  secondary  bulging  will 
take  place  at  this  point,  and  it  finally  ru})tures  there.  A  rupture  is  especially 
precipitated  by  high  blood-pressure,  such  as  occurs  on  exertion,  and  sud- 
den deaths  from  this  cause  are  quite  common  in  aneurism. 

When  the  wall  of  the  sac  presses  upon  neighboring  tissues  it  begins 
to  erode  them.  The  pressure  acts  in  the  following  way:  First,  it  cuts  off 
the  blood  supply  to  the  neighborhood  because  the  pressure  within  it  (aortic 
pressure)  is  greater  than  that  in  the  smaller  blood-vessels.  Secondly, 
necrosis  of  these  tissues  results  from  this  compression.  Thirdly,  the  products 
of  necrosis  are  absorbed  by  the  cells  in  the  tissues  of  the  very  vascular  wall 
of  the  aneurism  as  fast  as  they  are  produced.  Bone  tissue  too  is  absorbed 
by  the  activity  of  the  osteoclasts,  and  the  wall  of  the  sac  thus  advances 
gradually  through  the  chest  wall  very  much  as  a  tumor  might  do,  though 
without  the  intervention  of  abnormal  cells.  Thus,  the  aneurism  eats  its 
way  through  muscle,  cartilage,  bone,  nerves,  and  skin,  and  also  through 
the  walls  of  the  other  vessels  (pulmonary  artery,  vena  cava,  etc.),  bronchi, 
and  oesophagus,  always  forced  onward  in  a  straight  line  by  the  arterial 
pressure  in  the  aorta.  Hence,  aneurisms  usually  point  in  the  direction 
given  them  by  the  impact  of  the  blood  stream;  those  of  the  ascending  aorta 
pointing  to  the  right,  those  of  the  arch  pointing  upward,  those  of  the 
descending  arch  pointing  backward  and  to  the  left  (Fig.  301).  However, 
resistance  of  surrounding  tissues,  and  especially  local  thinning  of  the  aneu- 
rismal wall,  may  cause  its  course  to  be  deflected  somewhat  from  these 
typical  directions. 

Rupture. — The  excessive  thinning  which  results  in  perforation  fre- 
quently occurs  when  the  sac  has  just  penetrated  the  wall  of  one  of  the  sur- 
rounding structures, — bronchus,  oesophagus,  etc., — no  doubt  from  the  pres- 
ence of  local  infections  within  their  lumina,  and  sudden  death  may  result 
from  hemorrhage.  Or,  on  the  other  hand,  small  hemorrhages  may  occur 
from  the  erosion  of  smaller  bronchial  or  oesophageal  arteries  (see  page  529) 
or  through  the  wall  of  the  aneurism  without  any  such  immediate  results. 


528  DISEASES   OF   THE    HEART    AND    AORTA. 

The  growth  of  an  aneurism  after  penetrating  the  chest  wall  is  well 
shown  by  the  outlines  in  Fig.  302.  The  sac  becomes  larger  and  larger, 
secondary  sacculations  appear  upon  its  surface  (Fig.  302),  and  over  these 
the  thinned  skin  becomes  smooth,  tense,  glossy,  and  finally  of  a  reddish 


Fig.  301. — Composite  figure  showing  the  relations  of  various  aneurisms  to  surrounding  structures. 
(Schematic.)  OES,  oesophagus;  AN  SUBCL,  aneurism  of  the  subclavian  artery;  SUP.  V.  C,  superior 
vena  cava;  AN  INNOM,  aneurism  of  the  innominate  artery,  pointing  through  the  skin;  AN  TR,  aneu- 
rism of  the  transverse  portion  of  the  arch;  PHREN,  phrenic  nerve;  REC  LAR,  recurrent  laryngeal; 
L.  Fj4G,  left  vagus;  DA,  ductus  arteriosus  (Botalli);  A JV.  P. A.,  aneurism  of  the  pulmonary  artery;  LBR, 
left  bronchus;  AN.  SIN  VALS,  aneurism  arising  from  a  sinus  of  Valsalva;  AN.  R.  COR  and  AN.  L.  COR., 
aneurism  of  right  and  left  coronary  arteries;  AN  R.A,  aneurism  of  right  auricle;  AN.  L.V.,  aneurism  of  left 
ventricle.     The  arrows  show  the  directions  in  which  the  aneurisms  usually  point. 

or  brawny  hue.  The  whole  process  usually  requires  a  few  months,  but  it 
may  occur  more  rapidly.  On  the  other  hand,  in  a  case  described  by  Hirsh 
and  Robins  the  pulsating  tumor  upon  the  chest  remained  practically 
unaltered  in  size  for  twenty-five  years,  during  which  the  patient  continued 
to  do  heavy  w^ork.  Finalh%  however,  a  stage  is  reached  at  which  a  small 
perforation  appears,  oozing  blood,  and  soon  after,  with  a  rush  of  blood  Uke 


ANEURISM.  529 

the  bursting  of  a  dam,  the  aneurism  ruptures  and  the  patient  bleeds  to 
death  within  a  few  minutes. 

The  rupture  into  the  bronchus,  trachea,  or  oesoph- 
agus proceeds  in  the  same  wa}-.  There  is  usually  a  slight  premonitory 
haemoptysis.  This  generally  occurs  a  few  days  before  death,  but  may  not 
occur  until  a  few  hours  before  the  final  rupture ;  or,  as  in  the  case  reported 
by  Clarke,  it  may  be  present  for  months.  At  the  final  rupture  the  blood 
spurts  out  of  the  patient's  mouth  and  nose  and  may  even  be  projected 
several  feet  away  from  the  bed. 

On  the  other  hand,  when  the  aneurism  ruptures  inter- 
nally into  one  of  the  cavities  of  the  body,  the  symptoms  are  quite  differ- 
ent. The  patient  feels  something  giving  way  within.  Sudden  collapse, 
asthmatic  attack,  and  gradual  exsanguination  mark  rupture  into  the 
pleura.  Rupture  into  the  pericardium  is  attended  with  intense  pain, 
breathlessness,  collapse,  an  anginal  attack,  and  occasionally  a  con- 
vulsion. In  rupture  into  the  pericardium 
death    is    accelerated    by    cutting    off    the  /^'' 

venous  inflow,  just  as  in  simple  pericar- 
dial effusion,  only  within  a  minute  or  two. 
Of    course,    under    these    circumstances   no  a> 

blood   appears  externally. 

Rupture    of    the    aneurism    into 
the  pulmonary  artery,  vena   cav'a, 

.      -,    ,  .1  •    1  /  .    •    1  Fig.  302.— Tracings  of  the  outlines 

or    right    auricle    or  right  ventricle   some-        of  an  aneurism  of  the  innominate  artery, 

times  occurs.      The  symptoms  are  usuallv     showing  the  progress  of  its  growth  and 

~      ■,  .      "  the  formation  of  secondary  prommences 

sudden    onset    of    dyspnoea,    weakness,    often        upon   its  surface.      (Tracings  made  on 

collapse,  and  extreme  cyanosis,  which  ends     ,^°;;i  nitu^arsize.'  ^""^  °'"'  ^'^    ^""^ 
in  death  after  a  period  varying  from  sev- 
eral hours  to  several   months,  the  heart  being  unable   to   accommodate 
itself  to  the  sudden  changes  in  the  distribution  of  blood. 

However,  in  a  large  percentage  of  cases  (863  cases — 47  per  cent. — of 
Arnold's  1829  cases)  death  from  aneurism  is  not  due  to  rupture 
of  the  sac  but  "from  pressure  of  the  sac  upon  important  nerves  and  blood- 
vessels, or  from  secondary  changes  which  take  place  in  these  tissues  and  in 
other  vital  organs,  as  a  direct  or  indirect  result  of  such  pressure."  In  154 
cases  without  rupture  the  causes  of  death  were : 

Obstruction  to  air-passages 66 

Exhaustion 50 

Affections  of  lungs  and  pleura 2S 

Pericardial  affections 8 

Pressure  on  the  vena  cava  superior 1 

Collapse 1 

Clotting  within  an  Aneurism. — The  healing  of  an  aneurism  occurs  by 
clotting  within  the  sac.  Since  the  latter  is  lined  by  arterial  intima,  there 
is  under  ordinary  circumstances  no  more  reason  for  clotting  to  take  place 
there  than  elsewhere  in  the  artery.  As  shown  by  Mall  and  Welch,  arterial 
thrombosis  occurs  quite  suddenly  when  the  circulation  is  slowed  and  pulsa- 
tion disappears,  especially  if  there  is  some  injury  to  the  wall  of  the  artery, 
and  this  is  a  most  important  factor  in  bringing  about  thrombosis  within 
34 


530  DISEASES   OF   THE    HEART    AND    AORTA. 

an  aneurism,  though  some  fibrin  ferment  must  be  present.  As  a  rule,  in 
fusiform  aneurisms  the  circulation  is  too  strong  and  rapid  for  coagulation 
to  set  in,  but  in  sacculated  aneurisms  a  certain  amount  of  fibrin  collects 
along  the  wall.  Each  layer  of  fibrin  serves  as  a  filter  for  leucocytes,  from 
which  more  fibrin  ferment  is  generated  and  a  second  layer  laid  down,  and 
so  on  until  occasionally  the  entire  aneurism  may  be  filled  spontaneously 
by  a  laminated  clot. 

Owing  to  the  large  area  and  great  thickness  of  the  fibrin  deposited, 
and  to  the  fact  that  the  intimal  endothelium  is  in  most  places  still  intact, 
there  is  little  entrance  of  fibroblasts  into  the  clot  and  little  organization 
goes  on.  The  aneurismal  clot  is,  therefore,  not  converted  into  a  solid  mass 
of  connective  tissue  as  in  endarteritis  or  thrombo-angeitis  obliterans,  but 
remains  simply  laminated  fibrin.  Deposits  of  calcium  salts  sometimes 
occur  upon  them,  however,  and  tend  to  convert  the  obliterated  aneurism 
into  a  solid  tumor. 

SYMPTOMS. 

The  signs  and  symptoms  produced  by  aneurisms  vary  greatly,  and 
depend  upon  the  site  at  which  they  occur  along  the  aorta,  so  that  Broad- 
bent  has  been  "led  to  divide  thoracic  aneurisms  into  two  classes, — namely, 
aneurisms  of  physical  signs  and  aneurisms  of  symp- 
toms, from  the  predominance  of  physical  signs  and  symptoms  respec- 
tively,— the  former  term  applying  to  aneurisms  of  the  ascending  aorta 
and  first  part  of  the  arch,  the  latter  to  aneurisms  of  the  transverse  and 
descending  portions  of  the  arch." 

The  symptoms  produced  by  aneurisms  arise  secondarily  as  the 
result  of  pressure  upon  surrounding  structures.  Shortness  of 
breath  is  frequent,  resulting  both  from  pressure  on  the  trachea  and 
bronchi  and  from  concomitant  disturbances  in  the  circulation  (embarrass- 
ment of  heart  action,  stasis  from  pressure  on  veins).  Cough  is  a  common 
symptom,  from  pressure  upon  the  recurrent  larj-ngeal  nerves  as  well  as 
from  bronchitis  as  a  result  of  pressure  (occasionally  from  tuberculosis). 
The  pressure  on  the  laryngeal  nerve  causes  paralysis  of  the  corresponding 
vocal  cord  and  gives  the  cough  a  peculiar  metallic  quality  known  as  "the 
goose  cough,  brassy  cough,  stenotic  cough,  paretic  cough," 
etc.  It  is  really  the  cough  characteristic  of  paralysis  of  one  vocal  cord,  and 
it  is  characteristic  of  aneurism  only  in  so  far  as  that  the  latter  is  the  com- 
monest circulatory  disturbance  in  which  laryngeal  paralysis  is  a  symptom. 

Paroxysmal  dyspnoea  may  occur,  and  especially  in  certain 
postures  in  which  the  trachea  and  bronchi  are  pressed  upon  by  the  aneurism. 
This  ''asthma''  is  the  most  common  symptom  of  patients  presenting 
themselves  for  treatment,  and  careless  physicians  often  accept  its  presence 
as  the  final  verdict,  remaining  oblivious  to  the  true  nature  of  the  disease. 
Attacks  of  dyspnoea  or  suffocation  verj-  commonly  come  on  during  sleep 
when  the  laryngeal  muscles  relax  and  narrow  the  laryngeal  slit.  They 
occur  especially  when  the  patient  falls  into  an  unpropitious  position,  so 
that  he  soon  finds  it  most  convenient  to  sleep  bolstered  upright  and  leaning 
.slightly  forward  with  chin  depressed.  This  position  affords  the  maximum 
space  about  the  air-passages  with  the  minimum  of  tension  upon  them. 


ANEURISM.  531 

Not  infrequently  a  small  aneurism  of  the  arch  pointing  backward 
and  pressing  upon  the  trachea  or  bronchi  may  cause  actual  suffoca- 
tion, for  which  tracheotomy  may  be  necessary.  In  some  cases,  however, 
the  aneurism  may  be  situated  so  low  that  it  may  be  impossible  to  do  the 
tracheotomy  below  the  area  compressed.  The  only  possible  means  of  relief 
is  then  to  dissect  or  pull  the  aneurism  away  from  the  trachea,  or  to  intro- 
duce a  metal  tube  into  the  latter  and  thus  hold  the  trachea  open  at  the  point 
compressed.  This  procedure  is,  of  course,  extremely  difficult,  and  under 
all  circumstances  great  dyspnoea  from  pressure  on  the  trachea  is  in  itself 
a  dangerous  symptom. 

P  ain  is  a  common  symptom  in  aneurism,  and  may  be  of  three  kinds: 

1.  Angina  pectoris — reflex  referred  pain  over  the  heart  or  down  the  arm. 
This  is  especially  common  in  early  aneurism  at  the  beginning  of  the  ascending  aorta  and 
from  the  sinus  of  Valsalva,  and  is  probably  due  to  changes  in  or  pressure  upon  the  aortic 
plexus.    After  these  changes  have  been  long  established  this  pain  may  disappear  (Osier). 

2.  Sharply  localized  pain  may  arise  in  or  about  the  aneurism  itself  when 
its  walls  are  pressed  upon,  or  even  spontaneously,  and  especially  when  it  begins  to  erode 
the  chest  wall. 

3.  A  second  form  of  referred  pain  arises  without  reflex  mechanism  directly 
from  pressure  upon  the  intercostal  nerves  and  those  of  the  brachial  plexus,  especially  in 
aneurisms  of  the  transverse  and  descending  aorta.  The  latter  may  give  rise  to  pain  in  the 
back,  shoulder-blades,  and  sides  and  also  down  the  arm,  and  may  for  a  while  be  mistaken 
for  intercostal  neuralgia  or  for  the  pain  of  pleurisy.  Pain  down  the  ami  is  especially  com- 
mon when  the  aneurism  involves  the  innominate  or  subclavian  arteries,  particularly  when 
the  return  of  venous  blood  is  interfered  with  by  pressure  on  the  veins. 

Difficulty  in  swallowing  and  the  feeling  of  a  lump  in  the 
throat  may  result  from  pressure  upon  the  oesophagus,  especially  when  the 
aneurism  is  adherent  to  it  or  is  infiltrating  its  walls.  This  is,  of  course, 
characteristic  of  aneurisms  of  the  descending  portions  of  the  arch  and  to  a 
less  degree  of  the  descending  aorta.  It  is  not  at  all  a  rare  symptom,  and 
yet  is  by  no  means  as  common  as  might  be  expected  even  when  the  aneui'ism 
is  large. 

PHYSICAL    SIGNS. 

1.  The  presence  of  a  visible  mass  upon  the  chest  wall  or  elsewhere 
showing  a  pulsation  of  an  elevation  which  begins  about  0.05-0.10  second 
later  than  the  ventricular  systole  (or  the  first  heart  sound),  and  which  on 
palpation  is  felt  to  be  forcible  and  expansile  in  character  (i.e.,  presses 
outward  in  all  directions).  The  shock  with  the  first  sound  is  usually  well 
felt  and  often  accompanied  by  a  thrill;  and  a  diastolic  shock  accompanying 
the  second  sound  is,  when  present,  almost  characteristic'  On  auscultation 
there  is  usually  a  systolic  murmur  heard  over  the  aneurism,  and  occasionally 
a  diastolic  murmur  when  the  blood  flows  back  into  the  aorta  during  diastole, 
especially  through  a  narrow  opening.  This  is,  of  course,  most  common 
and  most  marked  when  aortic  insufficiency  is  present,  either  organic  or 
relative,  resulting  from  the  general  dilatation  of  the  aorta. 

Long  before  an  aneurism  perforates,  and  in  many  cases  when  it  is 
not  pointing  outward  but  upward  toward  the  episternal  notch  or  clavicles, 

*  The  writer  has  seen  one  case  of  hypernephroma  of  the  thigh  in  which  a  diastolic 
shock  was  palpable,  but  this  is  rare  even  in  the  most  vascular  tumors,  such  as  the  vascular 
mediastinal  sarcomata. 


532 


DISEASES   OF   THE    HEART    AND    AORTA. 


there  may  be  seen  a  diffuse  systolic  lifting  of  the  whole  chest 
wall  or  of  the  parts  above  the  tumor.  The  localized  heaving  is,  of  course, 
most  marked  when  the  aneurism  is  in  the  vicinity  of  cartilages  or  articu- 
lations in  the  chest  wall  and  in  younger  individuals;  while  the  most  diffuse 
heaving  occurs  in  the  portions  and  persons  where  the  ribs  and  sternum 
are  most  rigid.  The  impulse  thrill  and  shocks,  systolic  and  diastolic,  are 
also  frequently  present  when  no  heave  or  pulsation  can  be  seen. 

For  discerning  and  timing  slight  pulsations  the  writer  has  fre- 
quently found  it  convenient  to  hold  the  index  finger  a  few  millimetres 
away  from  the  chest  wall,  and  watch  for  either  a  periodic  narrowing  of 
the  slit  between  the  finger  and  the  chest  or  for  a  visible  movement  of  the 
shadow  cast  by  the  finger  upon  the  chest.    For  the  latter  purpose  the  light 

should  strike  as  nearly  as  possible  paral- 
lel to  the  chest  so  as  to  magnify  the 
movement  of  the  shadow  (Fig.  303). 

When  aneurism  is  suspected,  it  is 
particularly  important  to  ex- 
amine the  patient's  back  as 
well  as  to  inspect  carefully  the  front  of 
the  chest.  This  precaution  was  always 
particularly  emphasized  by  one  of  the 
great  teachers  of  medicine  who  also  un- 
intentionally illustrated  its  importance. 
On  one  occasion  he  and  another  pro- 
fessor, who  was  visiting  the  clinic,  dem- 
onstrated to  the  junior  students  a  case 
of  suspected  aneurism,  but  sent  him  to 
the  wards  for  X-ray  exanJination  with- 
out having  examined  the  back.  The  absolute  diagnosis  was  at  once  made 
by  the  house  officer,  who  in  the  routine  examination  discovered  a  well- 
marked  pulsation  at  the  back  at  the  level  of  the  third  thoracic  vertebra. 
Dulness  on  percussion  is  of  course  present  over  an  aneurism  as 
over  other  tumors,  the  note  being  fiat  when  the  tumor  is  near  the  surface, 
slightly  improved  when  it  is  deep.  This  improvement  is  often  very  slight 
in  deeply  situated  aneurisms  of  the  arch,  and  percussion,  especially  in 
the  first  right  and  left  interspaces  and  over  the  manubrium,  should  be 
very  carefully  carried  out  when  aneurism  is  suspected.  The  exact  outlining 
of  an  aneurism  by  percussion  may  be  very  difficult.  The  area  of  dulness 
on  even  the  lightest  percussion  may  be  considerably  greater  than  that  of 
the  aneurism  itself  (just  as  is  true  of  the  cardiac  dulness,  see  page  95). 
The  uniform  dilatation  of  the  aortic  arch  (to  about  twice  its  normal  diame- 
ter) which  is  so  frequent  in  aortic  insufficiency  may  give  an  area  of  dulness 
over  and  on  both  sides  of  the  sternum  which  may  lead  to  a  diagnosis  of 
aneurism  (Fig.  311).  The  true  nature  of  the  condition  can  be  shown  only 
by  the  X-ray  (Fig.  308). 

In  large  and  in  deeply  situated  aneurisms  direct  percussion  of  the  ver- 
tebral spines  by  Koranyi's  method  may  show  an  unusual  dulness  over  the  corre- 
sponding area  (especially  between  the  third  and  the  sixth  thoracic  spines)  and  may  prove 
of  assistance  in  establishing  the  diagnosis.    It  is,  of  course,  of  no  value  in  those  aneurisms 


t'^^ir- 


Fig.  303. — Method  of  inspecting  for  pulsa- 
tions. E,  eye  of  observer  looking  down  from 
above;  E',  eye  of  observer  upon  level  with 
pulsating  area;  finger  above  pulsating  area; 
<S  and  .S",  shadows  thrown  by  the  finger  upon 
the  pulsating  mass.  Solid  and  dotted  lines 
represent  the  outlines  of  the  pulsating  mass; 
arrows  indicate  the  extent  of  movement  seen. 


ANEURISM.  533 

of  the  arch  in  which  the  trachea  is  interposed  between  vertebrae  and  the  tumor.  The  heart 
is  occasionally  very  much  displaced  by  an  aneurism  which  may  itself  come  to  occupy  the 
usual  site  of  the  heart,  so  that  on  casual  examination  it  may  be  mistaken  for  the  latter. 
With  careful  auscultation,  however,  this  error  may  be  excluded. 

Pressure  upon  the  sympathetic  on  either  side  may  give  rise  to  inequality 
of  the  pupils,  usually  with  a  dilatation  upon  the  affected  side.  In 
late  stages,  however,  the  sympathetic  on  that  side  may  be  completely 
destroyed  and  the  pupil  then  becomes  smaller  on  the  affected  side. 
The  dilatation  is  best  seen  when  there  is  moderate  illumination,  for  in  strong 
lights  the  reflex  pupillar  constriction  may  overcome  the  dilator  action  of 
the  sympathetic. 

Tracheal  Tug. — W.  S.  Oliver,  who  described  the  sign  in  1878,  gave 
the  following  directions:  "Place  the  patient  in  the  erect  position  and 
direct  him  to  close  his  mouth  and  elevate  his  chin  to  the  fullest  extent; 
then  grasp  the  cricoid  cartilage  between  the  finger  and  thumb  and  use 
gentle  upward  pressure  upon  it;  when  if  dilatation  or  aneurism  exist  the 
pulsation  of  the  aorta  will  be  distinctly  felt  transmitted  through  the  trachea 
to  the  hand."  This  tracheal  tug  is  no  absolute  sign  of  aortic  dilatation. 
It  is  as  readily  produced  when  solid  mediastinal  tumors  or  enlarged  bron- 
chial glands  adhere  to  both  aorta  and  air-passages  as  from  aneurism. 

Sewall  finds  that  in  a  large  percentage  of  tuberculous  individuals 
(91  out  of  212 — 43  per  cent.)  a  slight  twitch  of  the  trachea  may  be  felt 
during  inspiration,  due  to  contraction  of  the  accessory  muscles,  but  this  is 
not  continuous,  not  synchronous  with  the  pulse-beat,  and  should  not  be 
mistaken  for  the  true  tracheal  tug.  Moreover,  in  his  large  series  of  obser- 
vations this  tracheal  twitch  of  non-aneurismal  origin  was  always  confined 
to  inspiration.  Sewall  found  it  particularly  common  in  cases  of  tuberculo- 
sis or  old  pleurisies  in  which  there  was  adhesion  to  the  left  pleura.  Medias- 
tinal adhesions  anchoring  the  aorta  to  the  air-passages  can  produce  it. 
Wenckebach  has  also  called  attention  to  the  fact  that  it  may  occur  in  cases 
of  enteroptosis,  in  which  the  heart  is  pulled  downward  with  the  liver,  and 
the  arch  of  the  aorta  thus  made  to  pull  upon  the  bronchi.  (This  is  well 
illustrated  by  the  patient  mentioned  on  page  602.)  The  tracheal  tug  is 
most  marked  in  inspiration. 

Tracheal  Percussion  Shock  (Smith). — H.  L.  Smith  has  found  that  if 
one  lightly  taps  the  chest  wall  (direct  percussion)  over  an  aneurismal  area 
one  feels  a  sudden  increase  in  the  impulse  as  soon  as  the  aneurismal  area 
is  reached,  a  shock  resembling  "the  sensation  experienced  by  one  when  a 
rubber  bag  filled  with  water  is  simultaneously  palpated  and  percussed  "  (semi- 
fluctuation).  The  fact  that  he  has  been  able  to  elicit  it  in  62  per  cent,  of  his 
cases  of  which  only  46  per  cent,  gave  a  tracheal  tug  indicates  the  usefulness 
of  the  sign.     In  certain  cases  it  is  undoubtedly  of  considerable  assistance. 

THE    PULSATION    AND    ARTERIAL    PULSE    IN    ANEURISM. 

The  pulsation  over  the  aneurism  resembles  the  form  of  the  arterial 
pulse  except  that  owing  to  the  elasticity  of  the  sac  the  rise  and  fall  are 
usually  more  gradual.  It  is  sometimes  of  importance  to  determine  whether 
the  pulsation  corresponds  to  an  aortic  aneurism  or  an  aneurism  of  the 
ventricle.    This  requires  the  most  carefully  timed  tracings  simultaneously 


534  DISEASES   OF   THE    HEART    AND    AORTA. 

from  apex  and  tumor.  If  the  pulsation  in  the  aneurism  begins  .07-. 09 
second  later  than  the  apex  beat,  the  aneurism  may  be  assumed  to  arise 
from  the  aorta.  If  it  arises  from  the  ventricle,  the  two  will,  of  course,  be 
synchronous.  On  the  other  hand,  as  occurred  in  a  case  still  under  the 
writer's  observation,  the  two  pulsations  may  be  absolutely  synchronous 
and  yet  X-ray  and  other  signs  may  show  that  the  aneurism  arises  from 
the  aorta. 

Delay  and  Inequality  of  the  Pulse. — Inequality  of  the  pulse  in  cases  of 
thoracic  aneurism  was  recognized  by  Harvey,  who  stated  very  correctly 
that  "the  pulse  in  the  corresponding  arm  was  small  in  consequence  of  the 
greater  portion  of  the  blood  being  diverted  into  the  tumor  and  so  inter- 
cepted." The  nature  of  this  inequality  was  made  the  subject  of  a  careful 
clinical  and  experimental  study  by  Marey  and  Frangois-Franck,  who  found 
that  when  an  aneurism  with  elastic  walls  occurred  along  the 
aorta  it  served  to  damp  the  oscillations  of  pressure 
in  the   arteries   nearest  to   it  and  thus  to  make  the  pulse  smaller 

in  these  arteries.     The  pulse-wave  thus 

[\    l\    (\    A      f\     f\     f\      f\        became  smaller  and  its  onset  less  sud- 

VENrVl/L/iyL  /Lj/ Vy  Lyl        ^^^^'    *^^    upstroke    becoming    very 

2  I  oblique  (pulsus  tardus). 

r\  \/\/\f\    ^/---■^4l>r--^Z^>:>..,,.--v^  Certain  aneurisms,  however,  have 

^       j^  \{2,  '"  no  effect  on  the  pulse,  and  it  may  be 

^  .    ^,  even  larger  upon  the  side  of  the  aneu- 

FiG.  304. — Effect  upon  the  Circulation  of  in-  .  ,  ,  i?c      ^     i       •  i 

terposing(A)aninelastic,and(B)anelasticbulb        HSm     tUaU    UpOU     the     Unattected     Side. 

along  the  course  of  an  artery  in  a  model  of  the     Marey   and    Fraucois  -  Frauck    showed 

circulation.     (Modified  from  Jrancois-lranck.)  •'           ,                     '                       •  (.        i 

1,  2    3    represent    successive    time   markings.  UpOU    their    models     that     if    the    SaC 

VENT,  pressure  cur\'e  within  the  model  of  the  -.vqs,     inplnqtip     fhp      niiltjp     wnvp 

ventricle;  .4ffT,  pressure  cur\e  within  the  model  ^^^^     ineiaSllC     ine      pUlSe-Wave 

artery.  A,  normal  artery.   The  elastic  siac  dimin-  WaS        iucrcased        On        the        af- 

i.-'hes  the  size  of  the  pulse,  delays  the  upstroke,  n           .         -i           •     ^                     A      'i-           V.             + 

and  delays  the  transmission  of  the  pulse-wave.  leCteCl      SlCie,      anCl     ItS     Character 

became    collapsing. 

Owing  to  this  damping  of  the  pulse-wave,  the  maximal  and  minimal  blood-pressures 
in  the  arteries  nearest  the  aneurism  tend  to  approach  the  mean  pressure,  so  that  the  maxi- 
mal pressure  may  be  from  5  to  30  mm.  lower  than  the  maximal  pressure  in  the  opposite 
arm,  though  there  may  be  a  considerable  difference  in  the  size  of  the  pulses  without  any 
marked  difference  in  maximal  or  minimal  pressures.  The  minimal  pressure,  being  already- 
nearer  to  the  mean,  is  less  affected  than  is  the  maximal,  and  often  no  difference  can  be  noted. 
Changes  in  the  size  and  in  the  quality  of  the  pulse  in  the  two  radial  arteries  are  much  more 
marked  to  the  palpating  finger  than  to  the  instrument,  for  the  slowed  circulation  may  be 
compensated  by  a  local  vasoconstriction  which  causes  a  smaller  pulse  without  appreciable 
change  in  the  pulse-wave.  The  pulse  is  usually  smaller  and  less  sudden  on 
the  side  nearest  the  aneurism,  and  hence  often  appears  to  be  retarded  when 
this  is  not  actually  the  case,  though  in  actual  fact  the  onset  of  the  pulse-wave  is  synchronous 
and  only  the  summit  of  the  pulse-wave  is  belated  (Frangois-Franck,  Marey,  v.  Ziemmsen) 
(Fig.  283).  Francois- Franck  and  Marey  showed,  however,  that,  both  in  man  and  in  the 
model,  the  presence  of  an  elastic  aneurismal  sac  along  the  aorta  caused  a  general  slowing 
in  the  transmission  of  the  pulse-wave  (apex  beat  —  radial  pulse  interval  =  0.2-0.22  second 
instead  of  0.12-0.14  second)'  in  all  the  arteries,  so  that  the  pulse-wave  in  both  radial 
arteries  begins  at  exactly  the  same  time.  When  the  aneurism  arises  not  from  the  aorta 
but  upon  the  innominate  or  the  subclavian  artery,  the  result  is  different.  The  pulse-wave 
in  the  aorta  now  advances  at  the  usual  rate  (apex  —  radial  =  0.12-0.14  second),  while  the 


'  In  cases  in  which  aortic  insufficiency  is  present,  especially  with  aneurisms  of  the 
ascending  arch,  this  delay  of  the  pulse-wave  is  not  present. 


ANEURISM. 


535 


IMIiMiHmiiM 


IV 


Fic.  305. — Effect  of  aneurisms  at  various  sites  upon  the  blood-pressure,  rate  of  transmission,  and 
the  form  of  the  pulse-wave.  (iSchematic.)  Bp,  blood-pressure  in  mm.  Hg ;  RR,  pulse  in  right  radial 
artery;  LR,  pulse  in  left  radial  artery.  I.  Aneurism  upon  innominate  artery.  II.  Aneurism  upon  the 
a.-^cending  aorta.  III.  Aneurism  upon  the  transverse  portion  of  the  arch  of  the  aorta.  IV.  Aneurism 
upon  the  left  subclavian  artery.  The  first  column  of  figures  indicates  blood-pressure  in  mm.  Hg ;  the 
second  column  indicates  the  transmission  time  of  the  pulse  wave  in  seconds.  The  figures  given  are  typical 
though  the  diflferences  are  larger  than  are  usually  encounteretl. 

transmis.sion  in  the  artery  from  which  the  aneurism  arises  is  slowed.  The  pulse-wave  is, 
therefore,  definitely  retarded  (0.05  to  0.07  second  later  than  in  the  other  radial),  in  some 
cases  even  when  there  is  no  difference  in  the  suddenness  of  the  upstrokes.  This  dif- 
ference in  the  time  of  the  pulse- waves  when  present  furnishes  a 
means  of  differentiating  between  aneurism  of  the  innominate  or 
subclavian  artery,  and  de- 
monstrates that  the  aorta  itself  is 
not  involved  (Francois  -  Franck). 
This  fact  may  be  of  great  practical 
importance  in  determining  the  oper- 
ative treatment,  especially  where 
the  shadow  cast  by  the  aneurism  lies 
close  to  that  of  the  aorta.  How- 
ever, this  delay  in  the  pulse  does  not 
occur  in  all  aneurisms,  but  only  in 
those  whose  walls  are  elastic, — the 
greater  number.  It  may  also  disap- 
pear as  clotting  occurs  along  the 
walls  of  the  aneurism,  and  the  elas- 
ticity of  the  sac  is  thus  lessened. 

In  view  of  these  facts,  it  is  evident  that  the  form  of  the  pulse  tracing 
is  of  no  more  value  than  the  simple  palpation  of  the  pulse  in  the  diagnosis 
of  aneurism,  and  the  only  graphic  method  of  practical  importance  is  that 
of  taking  simultaneous  tracings  from  both  radial  or  both  carotid   arteries 


Fig.  306. — Radial  pulse  tracings  from  tlie  right  and  left 
radial  arteries  of  a  patient  with  aneurism  of  the  first  part  of 
tlie  arch  of  the  aorta.  The  upstroke  of  the  pulse-wave  in  the 
right  radial  artery,  wliich  is  nearer  to  the  aneurism  than  the 
left,  is  more  gradual  than  that  in  the  latter. 


536 


DISEASES   OF  THE   HEART   AND    AORTA. 


in  cases  where  it  is  necessary  to  determine  whether  an  aneurism  is  confined 
to  the  innominate,  subclavian,  or  carotid  artery,  or  whether  it  also  involves 
the  aorta.  These  relations  often  cannot  be  shown  by  the  X-ray  and  rest 
upon  this  differentiation  alone. 


X-RAY    EXAMINATION. 


Most  of  the  things  which  are  inferred  from  physical  examination 
can  be  actually  seen  with  the  fluoroscope,  and  an  exactness  of  diagnosis 
can  be  reached  which  is  utterly  impossible  with  the  ordinary  methods.  In 
104  cases  of  aneurism  thus  examined  by  Baetjer,  the  cUnical  diagnosis  had 


been  correctly  made  in  70  per  cent. ; 
aneurism  in  20  per  cent.;  and  an 
been   discovered   with   the 


there  had  been  tentative  diagnosis  of 
unsuspected  aneurism  had 
X-ray  in  10  per  cent.  These 
findings  are  particularly  important, 
since  it  is  just  in  these  early  cases 
when  the  physical  signs  are  still 
indefinite  that  treatment  may  be 
profitably  instituted. 

However,  unless  certain  precau- 
tions are  taken  in  the  examination 
an  aortic  shadow  may  be  seen  which 
may  be  diagnosed  an  aneurism  even 
though  none  be  present.  This 
rounded  shadow  is  cast  by  the  arch 
of  the  aorta  just  to  the  left  of  the 
sternum,  and  it  may  be  specially 
marked  if  the  aorta  is  somewhat 
tilted,  as  sometimes  takes  place  in 
enteroptosis  (Wenckebach) .  Holz- 
knecht  has  shown,  however,  that 
this  error  will  not  be  made  if  the 
patient  is  also  turned  so  that  the 
rays  pass  from  left  back  to  right  front  (Fig.  81).  The  normal  aorta  thus 
lies  in  a  pla,ne  parallel  to  the  rays  and  is  seen  as  a  narrow  nearly  vertical 
band,  with  the  light  spaces  of  anterior  and  posterior  mediastinum  in  front 
and  behind  it.  The  uniformly  dilated  aorta  appears  as  a  wide  but  uni- 
form band.  The  aneurism  of  the  ascending  aorta  appears  as  a  battledore 
or  tennis  racket  with  handle  up,  the  aneurism  of  the  arch  as  a  racket  with 
handle  down.  Aneurisms  of  the  innominate  are  separated  from  the  aortic 
shadow  by  a  clear  space  which  is  bridged  by  the  narrow  shadow  of  the 
artery. 

As  Baetjer  states,  it  is  most  important  to  examine  the  chest  for  mal- 
formations and  for  misplacement  of  the  aorta  which  might  be  mistaken 
for  aneurism.  Persistence  of  the  ductus  arteriosus  (Botalli)  must  also  be 
considered  in  shadows  near  that  of  the  descending  arch.  The  shadow  of 
enlarged  mediastinal  glands  is  usually  speckled  or  blotchy  with  occasional 
lighter  areas,  rather  than  uniformly  dark,  while  the  edges  of  sarcomata 
and  other  solid  tumors  are  often  irregular  and  may  fade  away  gradually 


Fig.  307. — Radiograph  of  a  patient  with  a  large 
aneurism  of  ascending  aorta  and  the  arcli,  viewed 
from  behind.     (Kindness  of  Prof.  C.  M.Cooper.) 


ANEURISM. 


537 


into  the  surrounding- tissues.  Moreover,  unless  there  is  a  considerable 
degree  of  intrasaccular  clotting,  an  aneurism  will  be  seen  to  expand  during 
systole  and  to  contract  in  diastole,^  whereas  a  solid  tumor  will  at  most 
rotate  upon  its  axis. 

CHARACTERISTIC    FEATURES    OF    ANEURISMS    AT    DIFFERENT    SITES. 

Characteristic  features  of  thoracic  aneurisms  are  given  in  the  table 
below.  It  must  be  borne  in  mind,  however,  that  these  represent  the  con- 
ditions only  while  the  aneurisms  remain  relatively  small,  for  with  their  fur- 
ther growth  they  may  press  upon  other  structures  and  so  present  the  picture 
of  an  aneurism  affecting  a  different  part  of  the  aorta.  Large  aneurisms  also 
displace  the  heart,  and  may  even  occupy  the  usual  position  of  the  latter. 


Fig.  308. — Radiograph  of  a  patient  with  dif- 
fuse dilatation  of  the  arch  of  the  aorta.  (Kind- 
ness of  Prof.  C.  M.  Cooper.)  The  figure  also  shows 
dilatation  of  the  left  ventricle  and  slight  dilatation 
of  the  left  auricle. 


Fig.  309. — Diagram  of  the  radiograph  shown 
in  Fig.  308.  The  broken  lines  indicate  the  nor- 
mal outlines.  AO,  aorta;  OES,  oesophagus;  LV, 
left  ventricle. 


Aneurism  of  the  Heart. — Symptoms. — Indefinite  signs  of  cardiac  weak- 
ness. Physical  signs. — Two  points  of  maximal  impulse  over  which  tracings 
show  exactly  synchronous  pulsations  (this  point  is  far  from  pathogno- 
monic). Irregular  outline  of  cardiac  dulness  (encapsulated  pericarditis, 
pleurisy,  and  tumors  must  be  excluded) .  Sometimes  systolic  and  diastolic 
murmurs  over  heart  and  aneurism  not  present  over  aorta.  Pulse. — Feeble 
but  equal  and  not  delayed.  X-ray. — Bulging  of  shadow  of  ventricle  or 
auricle  with  enlargement  of  shadow  synchronous  with  systole  of  correspond- 
ing chamber.  Rupture. — Into  pericardium.  Death  often  from  cardiac 
weakness  or  coronary  sclerosis. 

Aneurism  of  Coronary  Arteries. — Symptoms. — No  characteristic  symp- 
toms. Occasional  cardiac  pain.  Physical  signs.  —  Arteriosclerosis.  No 
characteristic  signs  or  even  signs  of  illness.  (Aneurism  usually  size  of 
pigeon's  egg.)  X-ray.  —  No  abnormal  shadows.  Rupture.  —  Into  peri- 
cardium in  19  out  of  21  cases.     In  one  case  into  pulmonary  artery. 

Ascending  Aorta;  Intrapericardial  (Aneurism  of  Symptoms). — Symp- 
toms.— Angina  pectoris.     Attacks  of   cardiac   asthma.     Precordial  pains. 

^  Holzknecht  particularly  emphasizes  the  importance  of  using  the  lead  diaphragm 
in  examining  the  edges  of  the  shadow  for  pulsation. 


538  DISEASES   OF  THE    HEART    AND    AORTA. 

Pain  down  right  or  left  arm.  Shortness  of  breath.  Symptoms  of  cardiac- 
failure  predominate.  Physical  signs. — Distention  of  veins  of  head,  neck, 
upper  chest,  arms;  oedema  of  these  parts.  Tracheal  tug  absent  while 
aneurism  is  small.  Pupils  equal  if  aneurism  is  small.  Aneurism  usually 
small,  situated  in  second  and  third  right  interspaces.  Pulsation  in  second 
and  third  right  interspaces.  Often  signs  of  aortic  insufficiency.  General 
oedema  from  aortic  insufficiency.  Pulse. — Delay  of  pulse-wave  uniform. 
Pulses  may  be  equal  in  both  radials  or  may  be  smaller  in  either.  X-ray. — 
Inverted  racket-shaped  shadow  in  left  post,  to  right  ant.  illumination. 
Arch  of  aorta  clear.  Rupture. — Into  pericardial  cavity.  Pulmonary  arterj\ 
Right  auricle.  Superior  vena  cava.  (Esophagus.  I^eft  auricle.  Right 
ventricle.  Left  lung.  Right  lung.  Other  causes  of  death.  —  Dyspnoea. 
Exhaustion.  Hydrothorax.  Hydropericardium.  Bronchitis  and  pneu- 
monia.    Pulmonary  infarction.     Suffocation. 

Aneurism  of  the  Ascending  Aorta  between  Pericardium  and  Innominate 
Artery  (Aneurism  of  Physical  Signs). — Symptoms. — Slight  dyspnoea.  Pain 
when  aneurism  presses  on  or  erodes  chest  wall.  Often  an  accidental  finding. 
Physical  signs. — Flushed  face  with  dilated  veins;  sometimes  oedema.  Di- 
lated veins  of  arms.  Pulsation  in  second,  third,  and  fourth  right  interspaces 
(occasionally  shifting).  Dulness  to  the  right  of  the  sternum,  not  over  the 
manubrium.  Systolic,  sometimes  diastolic  murmur,  thrill  and  diastolic 
shock  over  aneurism.  Tracheal  tug,  if  aneurism  is  large.  Pulse. — Uni- 
form delay  of  pulse,  both  sides  synchronous.  Right  radial  usually  smaller 
than  left.  X-ray. — To  right  of  sternum  in  second  to  fourth  interspaces; 
best  made  out  in  post. -ant.  or  right  post,  to  left  ant.  illumination.  In  left 
post,  to  right  ant.  illumination  inverted  racket-shaped  shadow.  Compli- 
cations.— Often  aortic  insufficiency.  Bronchitis.  Tuberculosis  of  right 
lung.  Hemorrhage.  Right  hydrothorax.  Rupture. — Into  pericardium. 
Right  pleural  cavity.    Right  bronchus.    Right  auricle.    Superior  vena  cava. 

Aneurism  of  the  Innominate  Artery. — Symptoms. — Like  those  of  an- 
eurism of  arch  except  that  there  is  no  dysphagia  in  small  aneurisms.  Pain 
and  numbness  down  right  arm  and  to  right  shoulder.  Physical  signs. — 
Dilated  veins  and  swelling  over  right  arm  and  right  side  of  face.  Dulness 
extends  out  under  right  clavicle.  Pulsating  tumor  may  be  felt  under  the 
right  clavicle.  Paralysis  of  right  vocal  cord.  Right  pupil  in  early  stages 
larger  than  left.  Pulse. — Right  radial  pulse  smaller  and  definitely 
later  than  left.  X-ray. — A  v-shaped  shadow  is  seen  upon  the  left 
arm  of  the  V  Avhich  the  shadow  of  the  innominate  arteiy  makes  with  that 
of  the  aorta  on  left  post,  to  right  ant.  illumination.  Complications. — Right- 
sided  bronchitis.  Bronchopneumonia.  Tuberculosis.  Hydrothorax. 
Rupture. — Usually  points  upward  and  outward  toward  the  clavicle,  but 
may  point  downward  to  pleura  or  bronhci. 

Aneurism  of  the  Arch  of  the  Aorta  (Aneurism  of  Symptoms). — Symp- 
toms.— Change  in  voice,  especially  high  notes.  Brassy  cough.  Difficulty 
in  swallowing.  Pain  in  throat.  Dyspnoea,  sometimes  amounting  to  suffo- 
cation. Physical  signs. — Inequality  of  pupils.  Usually  dilatation  of  left 
pupil.  Dilated  veins,  flush,  and  sometimes  swelling  over  left  side  of  face, 
chest,  and  left  arm,  or  changes  bilateral.  Tracheal  tug  early.  Pulsation 
palpable  in  suprasternal  notch.     Pulsation  in  suprasternal  and  supraclavic- 


ANEURISM.  539 

ular  fossae.  Lifting  of  manubrium;  later  perforation  of  manubrium  or 
sternoclavicular  articulation.  Palpable  heaving,  systolic  and  diastolic 
.shocks,  and  often  thrill  over  manubrium.  Heart  sounds:  usually  systolic 
murmur  and  sometimes  diastolic  murmur  over  the  tumor.  In  aneurism 
beyond  the  innominate,  the  systolic  murmur  may  be  heard  in  the  left  car- 
otid and  brachial  but  not  in  the  right.  Bronchoscopy  may  show  tumor  per- 
forating bronchus.  X-ray. — Shadow  racket  shaped,  especially  seen  in  left 
post,  to  right  ant.  illumination.  Post. -ant.  or  ant. -post,  illumination  seen 
as  massive  shadow  above  that  of  the  heart.  Complications. — Bronchitis. 
Tuberculosis.  Suffocation  (asphyxia).  Inanition.  Rupture. — Externally 
(anteriorly  through  manubrium  or  above  clavicle).  Into  left  bronchus. 
Trachea.  Oesophagus.  Lungs  and  pleural  cavity,  pericardium,  mediasti- 
num. Pulmonary  artery.  Other  causes  of  death. — Exhaustion.  Pericarditis. 
Collapse.    Suffocation.    (Edema  of  larynx.    Pneumonia.    Tuberculosis. 

Aneurism  of  the  Descending  Aorta.' — Symptoms. — Lancinating  and  bor- 
ing pains  in  back,  left  shoulder,  left  side,  and  left  side  of  abdomen.  Stiffness 
of  back.  Shortness  of  breath.  When  the  aneurism  is  near  the  diaphragm, 
abdominal  pains  may  be  present  and  the  condition  may  be  considered  to  be 
abdominal.  Physical  signs. — Visible  pulsation  just  to  left  of  spinal  column. 
Dulness  on  percussion.  Heart  sounds  and  corresponding  shocks  over 
aneurism  and  tenderness  over  corresponding  spines.  Areas  of  hyper- 
a'Sthesia  or  analgesia  in  corresponding  spinal  segments.  Pulse. — Pulses 
.synchronous;  smaller  and  more  gradual  in  left  than  right.  X-ray.— 
cr-shaped  shadow  to  left  of  sternum,  especially  in  right  posterior  to  left 
anterior  illumination.  Complications. — Left-sided  bronchitis,  broncho- 
pneumonia, tuberculosis,  hydrothorax,  paraplegia  from  erosion  of  vertebra^. 
Rupture. — Backward  and  externally;  into  oesophagus,  left  pleural  cavity, 
right  pleural  cavity,  bronchi  and  lungs,  pulmonary  artery.  Other  causes  of 
death. — Pressure  on  trachea  and  bronchi,  exhaustion,  pneumonia,  and 
tuberculosis. 

The  following  histories  illustrate  typical  cases  of  aneurism: 

Ascending  Arch  above  Pericvrdium  (Aneurism  of  Physical  Signs). 

D.  N.  I..,  aged  4.5,  married.  Except  for  a  well-compensated  aortic  insufficiency  for 
the  past  eight  years,  with  slight  shortness  of  breath,  he  has  been  quite  healthy.  In 
November,  1903,  his  aneurism  was  discovered  accidentally  by  his 
brother,  who  is  a  physician. 

Examination  by  Dr.  Osier  revealed  a  well-nourished  man  who  does  not  appear  ill. 
F^ace  a  little  congested,  veins  of  neck  and  arms  full;  pulse  48  per  minute,  both  apparently 
synchronous,  a  little  larger  on  left  than  on  right  (maximal  pressure:  left  arm  140;  right 
arm  125).  There  is  no  tracheal  tug.  Over  the  thorax  a  wavy  impulse  is  seen  in  all 
the  right  interspaces  above  the  liver,  and  an  area  of  dulness  as  outlined  in  Fig.  :U0,  A.  Rela- 
tive cardiac  dulness  in  fourth  interspace  extends  16. o  cm.  to  left  and  15  cm.  to 
right  of  midline.  Over  the  aneurismal  area  there  is  a  marked  systolic  thrill  and  murmur; 
over  the  heart  a  svstolic  and  diastolic  murmur. 


'  In  120  cases  of  aneurism  of  the  descending  aorta  collected  from  the  literature  Milanoff 
fovmd  pain  in  72,  dysphagia  in  20,  haematemesis  13,  hsemoptysis  21,  left-sided  pleural  effu- 
sion in  a  few  cases.  Andreef  found  only  S  cases  of  paraplegia  from  aneurism  in  the  litera- 
ture.   The  iluration  is  often  from  10  to  15  years;  longer  than  that  of  aneurisms  elsewhere. 

The  condition  is  very  well  discu.ssed  in  English  by  Osier  and  more  recently  by  Hewlett 
and  Clark,  who  give  excellent  radiographs  and  a  very  useful  summary  of  the  literature. 


540 


DISEASES   OF   THE   HEART   AND    AORTA. 


X-ray  examination  by  Dr.  Baetjer  showed  the  pulsating  shadow  of  an  aneurism  of 
size  corresponding  to  the  area  obtained  on  percussion,  arising  from  the  ascending  arch  of 
the  aorta. 

Patient  left  the  hospital,  and  one  month  later  died  without  warning  while  asleep. 
The  only  signs  of  the  approaching  end  were  fifteen  minutes  of  stertorous  breathing. 
Autopsy  revealed  a  large  aneurism  corresponding  to  that  diagnosed  clinically,  as  well  as 
arteriosclerosis  and  aortic  insufficiency.    There  is  no  note  of  rupture  of  the  aneurism. 


Fio.  310. — Cardiac  dulness  in  cases  of  aneurism.  A.  Ascending  aorta  (D.  N.  L.).  B.  Subclavian 
artery  (J.  B.):  the  shaded  area  indicates  the  tumor,  the  curve  indicates  the  pulsation.  C.  Second  part 
of  the  transverse  portion  of  the  arch  (K). 


Aneurism  of  Innominate  Artery. 

J.  B.,  aged  44.    Had  syphilis  13  years  ago,  otherwise  healthy. 

Two  years  ago  complained  of  aching  in  right  shoulder  and  right  side  of 
neck  down  arm  to  hand.  No  pain  in  chest.  There  were  swelling  of  feet  and  ankles  and 
shortness  of  breath.  About  this  time  he  began  to  have  troublesome  paroxysms  of 
coughing.  In  May,  1903,  noticed  that  his  V o i c e  was  ''cracked.''  In  August, 
1903,  he  noticed  a  pulsating  swelling  above  the  right  clavicle.  This  was 
diagnosed  as  aneurism  of  the  innominate,  and  the  right  carotid  was  ligated 
above  the  tumor.     The  subclavian  could  not  be  ligated,  as  the  patient  took  chloroform 


ANEURISM.  541 

badly.  After  the  ligation  the  tumor  rapidly  increased  in  size.  When  he  entered  the  Johns 
Hopkins  Hospital  two  months  later,  his  voice  was  husky,  the  right  pupil  was  larger  than 
the  left  (irritation  of  the  right  sympathetic  ganglia),  and  a  large  rounded  pulsating  tumor 
was  seen  occupying  the  position  of  the  manubrium  and  extending  out  along  the  right 
clavicle  (Fig.  310,  A,  B).  The  prominence  of  this  tumor  is  shown  in  Fig.  302.  Over  the 
tumor  a  well-marked  systolic  and  diastolic  shock  may  be  felt.  The  two  heart  sounds  are 
heard  over  the  tumor.  There  is  some  resonance  on  percussion  between  the  tumor  and  the 
heart.  The  area  of  cardiac  dulness  is  not  enlarged,  but  a  soft  diastolic  murmur  is  heard 
at  apex  and  base.  The  right  radial  pulse  is  smaller  than  the  left  and  a  little  delayed.  The 
blood-pressure  varied,  at  first  being  160  in  left  arm,  140  in  the  right  brachial,  later  reach- 
ing 150  in  right  and  130  in  left. 

Patient  was  seen  by  Dr.  Finney,  but  wiring  and  other  operative  procedures  were 
considered  impracticable.  He  was  kept  at  rest  in  bed  on  restricted  diet,  but  nevertheless 
the  aneurism  grew  rapidly,  as  shown  by  the  successive  elevations  in  Fig.  302. 

On  Dec.  2,  at  4.00  a.m.,  he  felt  a  severe  throbbing  in  the  aneurism,  and  a  couple  of 
smaller  bulgings  (Fig.  302)  appeared  upon  its  surface,  which  had  not  been  present  the 
day  before,  and  the  whole  aneurism  appeared  to  be  definitely  larger.  The  patient  insisted 
upon  leaving  the  hospital  at  once  to  return  to  his  home  in  South  Carolina. 

Aneurism  of  the  First  Part  of  the  Transverse  Arch  of  the  Aorta. 

J.  D.,  an  unmarried  sailor,  aged  37,  entered  the  Johns  Hopkins  Hospital  on  Jan.  5, 
1909,  complaining  of  pain  in  the  chest  and  inability  to  sleep.  He  had  had  no  infectious 
diseases  except  gonorrhoea,  denied  spyhilis,  and  gave  no  history  of  secondaries.  Except  for 
occasional  sprees,  he  uses  alcohol  in  moderation.    As  a  sailor  he  has  always  done  heavy  work. 

He  was  well  until  about  four  months  before  admission,  when  he  had  an  attack  of 
"heavy  pressure"  and  tightness  across  his  chest  at  night,  and  some  weeks  later  stinging 
pains  in  his  chest  3-4  cm.  above  the  xiphoid  process,  which  seemed  to  radiate  to  both 
sides  of  the  chest  and  to  pass  through  to  the  back.    The  pressure  kept  him  from  sleeping. 

Upon  examination  the  veins  upon  the  left  side  of  the  neck  were  found  to  be  dilated, 
and  the  veins  were  much  more  prominent  than  on  the  right.  There  was  no  tracheal  tug. 
There  was  an  area  of  dulness  behind  the  medial  end  of  the  right  clavicle,  the  manubrium, 
and  the  medial  half  of  the  left  clavicle,  which  was  continuous  with  the  upper  border  of 
cardiac  dulness.  The  left  radial  pulse  was  somewhat  smaller  than  the  right  and  seemed 
to  be  a  trifle  retarded.  •  Maximal  pressure  in  the  right  radial  ranged  from  115  to  130  mm. 
Hg,  in  theleft  from  85  to  110  mm.  Hg. 

Fluoroscopic  examination  by  Dr.  Baetjer  showed  a  pulsating  tumor  about  the  size 
of  a  hen's  egg  projecting  almost  entirely  to  the  left  of  the  sternum  opposite  the  first  and 
second  interspaces  (transverse  portion  of  the  arch  of  the  aorta). 

The  patient  was  discharged  somewhat  improved  after  a  short  sojourn  in  the  hospital. 

Aneurism  of  the  Left  Side  of  the  Transverse  Arch. 

H.  D.  K.,  brush-maker,  aged  49,  admitted  to  the  surgical  service  of  the  Johns  Hopkins 
Hospital  on  March  14, 1908,  complaining  of  aneurism.  Family  history  was  negative.  He  had 
been  perfectly  healthy  all  his  life  except  for  an  attack  of  pleurisy  six  years  before  admis- 
sion, an  attack  of  gonorrhoea  at  19,  and  a  chancroid,  not  followed  by  secondaries,  at  25. 

Two  weeks  before  admission  he  felt  a  burning  pain  in  the  left  chest  and 
had  some  shortness  of  breath,  both  of  which  have  become  worse  since  then.  He  sometimes 
is  awakened  with  shortness  of  breath  and  precordial  pain.  For  the  past  year  his  voice  has 
been  husky,  a  condition  which  set  in  suddenly  after  violent  exertion  while  splitting  wood. 

He  is  a  well-nourished  man  of  rather  anxious  expression.  The  pupils  are  equal  and 
react  to  light  and  accommodation.  There  is  a  well-marked  tracheal  tug.  Chest  expansion 
is  slight  on  respiration.  There  is  a  definite  pulsation  over  the  first  left  interspace  and 
sternoclavicular  junction,  in  which  area  the  shocks  accompanying  the  two  sounds  are 
readily  palpable. 

Note  by  Dr.  Bnggs. — H  e  a  r  t  :  Maximal  impulse  in  fifth  left  interspace  11  cm.  from 
midsternal  hne;  dulness  extends  to  this  point  on  left,  reaches  above  to  middle  of  third 
rib,  and  on  right  2.5  cm.  in  third  left  interspace.  Cardiohepatic  angle  is  normal.  There 
is  dulness   behind   the    manubrium,  extending  to  left,  as  per  diagram,  8.5  cm. 


542  DISEASES   OF   THE    HEART    AND    AORTA. 

in  first  interspace  and  below  to  second  interspace,  on  the  right  to  just  beyond  the  sternal 
margin.  On  palpation  over  the  thill  area  there  is  a  strong  lifting  pulsation, 
maximal  at  a  point  5.5  cm.  to  left  and  definitely  expansile.  No  thrill  felt.  Diastolic  shock 
well  marked.  At  apex  and  inward  toward  the  base  there  is  a  very  short  systolic  murmur, 
which  is  not  transmitted  beyond  the  border  of  the  heart.  First  sound  is  rather  tapping 
at  apex.  Along  the  left  sternal  border  this  murmur  increases  in  intensity  and  is  maximal 
over  the  mass  above  the  heart  at  the  point  of  greatest  pulsation,  where  there  is  a  well- 
marked  systolic  bruit  followed  by  a  ringing  second  sound.  A  very  faint  systolic  murmur 
is  heard  at  the  aortic  ring,  and  the  second  sound  is  clear.  No  diastolic  murmur.  The 
second  pulmonic  is  louder  than  the  second  aortic.  The  pulse  is  of  gootl  volume,  regular, 
rather  high  tension,  and  not  collapsing.  Vessel  wall  definitely  thickened.  Some  cyanosis 
of  finger-tips  and  lips.  The  volume  of  the  pulse  on  the  right  side  is 
decidedly  larger  than  on  the  left.  There  is  a  circimiscribed  area  of 
dulness  in  the  left  interscapular  region  in  which  percussion  note  has 
a  peculiar  wooden  tympany  like  that  over  consolidated  lung.  Over  this  area  the  breath 
sounds  are  rather  more  intense  than  over  the  rest  of  the  lung  but  they  are  not  tubular 
in  character. 

On  January  20  the  aneurism  was  wired,  under  Schleich  solution  anaesthesia,  by  Dr. 
Finney,  with  twelve  feet  of  silver-copper  wire,  through  which  a  10-MA  current  was  passed 
(Moore  Corradi  method).  Clotting  took  place  promptly.  The  patient  stood  the  opera- 
tion well.  The  patient  was  considerably  relieved  as  regards  pain,  but  the  pulsation  soon 
returned. 

Aneurism  of  the  Descendixg  Aort.\. 

Notes  of  the  following  case  are  taken  from  the  records  of  the  Johns  Hopkins  Hospital : 

Ch.  L.,  colored  laborer,  aged  48,  was  first  admitted  to  the  Johns  Hopkins  Hospital 
on  October  14,  1898,  complaining  of  pain  in   the  back,  left  side,  and  abdomen. 

His  family  history  was  negative.  He  had  always  been  healthy,  but  had  measles, 
whooping-cough,  tertian  malaria,  and  at  17  had  syphilis  which  was  not  adequately 
treated.  He  has  done  a  great  deal  of  hard  work  on  a  farm,  has  drunk  a  great  deal  of  whiske>-, 
and  smoked  heavily. 

His  present  trouble  began  suddenly  about  four  years  ago,  when  he  was  seized  with 
a  severe  pain  in  the  lower  left  abdomen.  This  lasted  a  couple  of  weeks.  It  was 
always  relieved  when  his  thighs  were  flexed  upon  the  abdomen,  and  was  always  increased 
after  exposure  to  bad  weather.  Four  years  after  this  a  pain  in  the  left  side  of  the 
back  appeared,  which  has  gradually  increased.  This  also  is  relieved  by  flexing  the  thighs. 
For  the  past  six  years  he  has  passed  blood  in  the  stools  during  periods  when  the  i)ain  in 
the  left  flank  was  worse. 

A  note  by  Dr.  Futcher  at  that  time  states,  that  "  the  patient  was  found  lying  in  bod 
on  the  left  side  with  the  knees  flexed.  Pupils  are  of  normal  size,  equal,  and  react  to  light 
and  accommodation.  The  lung  expansion  and  vocal  fremitus  are  diminished  over  the 
entire  left  lung,  and  the  breath  sounds  were  exaggerated  in  front  and  in  the  axilla.  There 
were  a  few  moist  rales  in  the  third  and  fourth  left  interspaces.  Behind,  the  breath  sounds 
are  very  indistinct  below  the  angle  of  the  scapula.  The  percussion  note  was  found  to  be 
impaired  over  the  entire  left  front  as  far  down  as  the  fifth  rib  and  over  the  entire  left 
back,  being  flat  below  the  angle  of  the  scapula. 

Heart. — The  maximal  impulse  was  seen  in  the  fifth  interspace  7.5  cm.  from  the  mid- 
line, but  dulness  extended  3  cm.  to  the  left  of  this  point.  Both  the  first  and  second  sounds 
were  reduplicated. 

The  liver  was  slightly  enlarged;  the  spleen  just  palpable.  There  were  no  masses  nor 
areas  of  tenderness  in  the  left  flank  to  accovmt  for  the  pain. 

On  Oct.  21  Dr.  Futcher  noted  a  definite  heaving  of  the  entire  body  of  the  sternum 
and  a  well-marked  systolic  retraction  in  the  eighth,  ninth,  and  tenth  left  interspaces  be- 
hind. A  tracheal  tug  was  present,  but  the  vocal  cords  were  not  paralyzed.  The  pulse  wa.s 
equal  on  the  two  sides. 

In  spite  of  rest,  restricted  diet,  and  potassium  iodide  and  repeated  gelatin  injections, 
his  pain  in  the  back  gradually  became  worse,  compelling  him  to  seek  relief  by  lean- 
ing over  tbe  back  of  the  chair.  It  became  so  severe  that  it  was  not  relieved 
by  30  mg.  (gr.  ss)  of  morphine.  However,  later  in  his  stay  his  condition  gradually  became 
better  and  the  pain  became  a  little  less  frequent  and  less  intense. 


ANEURISM. 


543 


There  was  very  little  change  in  his  condition  between  that  time  and  March,  1902, 
when  for  the  first  time  there  was  noted  a  definite  systolic  pulsation  in  the  left 
interscapular  region  which  gradually  increased  until  it  involved  three  ribs  and  interspaces. 
His  condition  gradually  became  worse.  Respiratory  movement  almost  entirely  disappeared 
upon  the  left  side  and  a  scoliosis  developed  with  concavity  toward  the  right.  The  area 
of  cardiac  dulness  increased  to  the  right,  where  pulsation  was  particularly  well  marked 
and  a  superficial  scratchy  systohc  murmur  was  heard  over  the  precordium.  His  pain 
became  so  intense  that  he  could  but  rarely  lie  down.  An  area  of  absolute  analgesia  devel- 
oped in  the  sixth  and  seventh  left  interspaces,  impaired  sensibility  to  heat,  cold,  and  pain 
being  found  in  the  fifth  interspace  as  well.  About  this  time  he  began  to  feel  pain  on  swal- 
lowing, referred  to  the  middle  of  the  sternum. 

During  the  night  of  Oct.  25  he  complained  of  pain  and  intense  shortness  of  breath, 
and  suddenly  vomited  about  50  c.c.  of  bright  red  blood.  Ten  minutes  later  he 
vomited  25  c.c.  more  blood.  He  was  quieted  with  morphine  during  the  night,  but  in  the 
early  afternoon  of  the  twenty-fifth  he  vomited  about  500  c.c.  of  blood  within  three  minutes, 
became  pulseless,  and  died. 

At  autopsy  the  heart  was  found  to  be  displaced  to  the  right  (extending  8  cm.  to 
the  right  of  the  midline)  by  a  tremendous  aneurismal  sac  18X14X9  cm.  This  sac  was 
fusiform  with  sacculations  at  its  upper  and  lower  ends.  It  arose  from  the  descending 
part  of  the  arch  and  the  descending  aorta  itself  and  pointed  backward, 
eroding  the  bodies  of  all  the  thoracic  vertebrae  from  the  fifth  to  the  tenth  as 
well  as  the  seventh,  eighth,  and  ninth  ribs.  The  erosion  of  the  intervertebral  disks  was 
much  less  marked.  The  aneurismal  sac  also  compressed  the  oesophagus  at  the  level  of  the 
bronchial  bifurcation,  where  it  eroded  through  the  oesophageal  wall,  making 
an  opening  2.5  cm.  in  diameter.  "The  edges  of  this  aperture  were  ragged  and  necrotic; 
the  tissue  about  it  dark  gray-green  in  color." 

The  aneurismal  sac  was  partly  filled  by  a  large  lamellated  clot. 

The  ascending  aorta  was  dilated  and  atheromatous;  the  descending  aorta  below  the 
aneurism  likewise. 

The  heart  was  much  enlarged;  the  walls  hypertrophic;  the  valves  normal. 

There  were  many  pericardial  adhesions,  especially  firm  over  the  left  auricle  and  the 
coronary  veins,  and  there  were  tortuous 
patches  over  both  ventricles. 

The  stomach  contained  a  litre  of 
clotted  blood.     Other  organs  normal. 


Simple  Dilatation  of  the  Arch. 

L.  D.,  gardener,  aged  55,  native 
of  Ireland,  came  to  the  .Johns  Hopkins 
Hospital  Dispensary  on  July  13,  1909, 
complaining  of  pain  on  swallowing  and 
trouble  in  passing  water. 

The  family  history  was  negative. 
The  patient  had  smallpox  at  18,  gon- 
orrha?a  at  35  and  again  at  48,  and 
a  chancre  at  35  followed  by  definite 
secondary  manifestations,  for  which 
he  had  been  given  medicine  by  mouth. 
He  has  drunk  whiskey  in  excess  and 
has  done  a  good  deal  of  heavy  work. 

He  was  perfectly  healthy  until  the  past  ten  days,  since  when  he  feels  food  passing 
down  his  oesophagus  and  has  a  little  pain  which  is  referred  to  the  level  of  the  cardia.  He 
vomits  immediately  after  eating,  but  can  swallow  liquids  without  difficulty. 

Examination  reveals  a  fairly  nourished  man  of  ruddy  complexion  with  some  dilated 
venules.  The  left  pupil  is  somewhat  larger  than  the  right,  though  both  react  to  light  and 
accommodation.  There  is  a  slight  but  definite  tracheal  tug;  no  tracheal  percussion  sliock. 
There  is  no  glandular  enlargement.  The  lungs  are  clear  except  for  a  few  widely  scattered 
piping  rales. 


Fig.  311. — Area  of  cardiac  dulness  in  a  patient  (I..  D.> 
with  dilated  arcli  of  the  aorta. 


544  DISEASES   OF   THE    HEART    AND    AORTA. 

The  heart  is  not  enlarged;  apex  in  fifth  left  interspace  10  cm.  from  the  midline.  Dul- 
ness  extends  4.5  cm.  to  the  right.  The  relative  dulness  is  continuous  above  with  a  strip 
3.5  cm.  upon  either  side  of  the  sternum,  over  which  the  percussion  note  is  very  slightly 
impaired.  This  area  extends  up  as  far  as  the  upper  border  of  the  second  rib,  and  is  shown 
by  the  fluoroscope  to  correspond  with  a  uniform  shadow  of  the  dilated  aortic  arch.  The 
heart  sounds  are  clear;  the  second  aortic  distinct;  no  diastolic  murmur  present.  Pulse 
is  of  good  volume,  not  collapsing. 

Abdomen  shows  no  masses ;  no  visible  peristalsis.  There  are  no  tenderness  and  no  ab- 
normalities palpable.  The  stomach  tube  is  passed  into  the  stomach  without  difficulty, 
and  a  very  small  amount  of  clear  fluid,  free  from  HCl,  obtained;  lavage  fluid  clear.  Des- 
moid test  negative.  He  was  given  alkaline  gentian  tincture  +  strychnine  (1  mg.  =  ^V  gr.) 
before  meals,  under  which  treatment  his  symptoms  rapidly  diminished. 

Diagnosis  :  Chronic  alcoholic  gastritis,  anacidity,  dilatation  of  the  aortic  arch. 

Aneurism  of  the  Abdominal  Aorta. 

M.  P.,  machine  agent,  aged  30,  was  first  admitted  to  the  Johns  Hopkins  Hospital 
on  Oct.  31,  1899,  complaining  of  kidney  and  stomach  trouble.  The  family  his- 
tory was  negative. 

The  patient  had  had  measles,  chicken-pox,  mumps,  and  whooping-cough,  typhoid 
fever  at  23,  followed  by  pain  in  the  ankles  and  knees.  He  had  gonorrhoea  two  years  before 
admission  (about  one  year  before  the  onset  of  the  present  trouble),  but  denies  lues.  He 
worked  on  a  farm  until  his  attack  of  typhoid  fever,  since  when  he  has  not  been  strong. 
He  does  not  drink  nor  smoke  and  is  a  hearty  eater. 

The  present  illness  began  six  months  before  admission,  with  some  soreness  and  pain 
in  the  abdomen,  which  had  no  relation  to  the  taking  of  food  except  that  it  was 
more  intense  after  a  large  meal.  He  vomited  occasionally  but  rarely.  The  pain  was  at 
first  a  sharp  throbbing  pain  in  the  left  side.  It  was  so  severe  as  to 
cause  him  to  remain  in  bed  for  a  period  of  three  months,  during  which  he 
had  to  be  given  morphine.  After  the  three  months'  sojourn  in  bed  the  pain  became  less, 
and  he  was  almost  free  from  symptoms  for  about  six  weeks,  when  he  was  taken  with  a 
sudden  sharp  cutting  pain  in  the  right  side  just  under  the  ribs,  running 
around  toward  the  right  and  down  toward  the  testicle. 

On  examination  he  was  found  to  be  a  well-nourished  man  of  rather  sallow  color. 
There  was  no  glandular  enlargement.  The  lungs  were  clear  on  auscultation  and  percussion. 
The  heart  was  not  enlarged;  the  heart  sounds  clear. 

In  the  abdomen  there  was  a  very  well-marked  pulsation  visible  in  the  epi- 
gastrium. There  was  dull  tympany  over  this  area,  and  inflation  of  the  stomach  showed 
that  the  pulsating  mass  was  covered  by  the  latter.  There  was  considerable  tenderness 
over  the  pulsating  area;  Dr.  Osier  was  able  to  make  out  a  definite  soft  systolic  mur- 
mur, and  on  Nov.  5  with  the  deepest  possible  palpation  could  make  out  a  definite  mass 
with  expansile  pulsation.  The  case  was  diagnosed  as  abdominal  aneurism 
and  wiring  was  advised.    This  was  performed  by  Dr.  Finney  two  months  later. 

Note  by  Dr.  Finney. — An  incision  was  made  2.5  cm.  befow  the  xiphoid.  The  stomach 
was  retracted  downward;  the  lesser  peritoneum  was  opener!.  The  pancreas 
covered  the  lower  surface  of  the  tumor.  Attempt  was  niade  to  dissect  the  pan- 
creas. This  was  abandoned  on  account  of  profuse  and  persistent  hemorrhage. 
The  incision  was  then  enlarged  upward,  the  edge  of  the  liver  elevated,  and  the  tumor 
exposed  above  and  to  the  right  of  the  pancreas.  A  needle  was  inserted  at  this  point  to  a 
depth  of  3-4  cm.  and  8-9  feet  of  silver  and  copper  alloy  wire  introduced.  Ten  milliamperes 
of  current  were  passed  for  one  hour.  The  needle  was  withdrawn,  the  wire  cut  close  to  the 
aneurismal  sac  and  turned  in  with  a  clamp.  No  bleeding.  One  or  two  bleeding  points 
about  the  pancreas  were  tied  with  fine  silk.  The  incision  was  closed.  The  patient  made 
an  uneventful  recovery  and  experienced  considerable  relief  from  pain,  so  that  nine 
months  later  it  gave  him  little  trouble,  though  the  aneurismal  pulsation  was  still 
expansile.     There  was  now  aloud  systolic  murmur  over  the  mass. 

The  pain,  however,  gradually  returned  and  never  left  him.  It  was  so  severe  that  he 
was  a  frequent  visitor  at  the  hospital  and  was  compelled  to  use  a  good  deal  of  morphine. 
He  was  admitted  to  the  writer's  ward  in  Jan.,  1904,  somewhat  worse  than  at  any  time 
previously.     The  aneurismal  mass  now  extended  from  the  ensiform   to   within    3 


ANEURISM.  545 

centimetres  of  the  umbilicus.  Its  surface  was  smooth  and  no  areas  of  bulg- 
ing could  be  made  out. 

On  Jan.  7  the  leucocytes  were  5000;  the  hajmogolobin  90  per  cent.  He  was  quite  well 
(when  given  morphine)  until  the  night  of  Jan.  21,  when  he  had  asudden  attack  of 
most  intense  pain  in  the  lower  back  and  abdomen,  "causing  him  to  cry  out  and  toss 
about,  arching  his  back  and  stiffening  all  his  muscles  in  his  attempts  to  bear  the  pain  in 
silence."  There  was  no  objective  change  in  the  abdomen,  but  the  tenderness  over  the 
aneurism  was  more  marked  than  before. 

The  next  day  he  had  several  attacks  of  pain  and  vomiting.  At  4.00  p.m.  the  vomit- 
ing was  very  severe  and  was  accompanied  by  intense  pain  and  sudden  collapse. 
His  color  became  a  ghastly  pallor.  He  became  almost  pulseless  before  any  one  could 
reach  him.  He  was  still  conscious  and  complained  of  great  pain  in  the  back  and 
right  side  of  the  abdomen,  to  relieve 
which  .15  Gm.  (gr.  iiss)  of  morphine 
were  necessary,  given  within  an  hour. 
At  5.45  p.  M.  a  small  saline  infusion 
was  given  and  caused  the  pulse  to 
improve  slightly.  Strychnine,  2  mg. 
(sV  gr-))  +  digitalin  (German),  .15  mg. 
(tV  gr),  had  no  effect.  The  maximal 
blood-pressure  before  the  collapse  was 
130  mm.  Hg,  after  it  was  70  mm.  Hg. 

The  next  day  there  was  dulness 
throughout  the  right  flank  extending 
up  to  liver  dulness  (due  to  outpouring 
of  blood  into  the  peritoneal  cavity). 
The  systolic  murmur  over  the  tumor 
disappeared,  but  the  aneurismal  mass 
still  pulsated.  The  haemoglobin  was 
found  to  have  fallen  to  55  per  cent.; 
the  leucocytes  rose  to  17,500. 

During  the   next   few  days   the 

patient's  condition  seemed  to  improve.  ^'S-  ^A^'l'^"™?'"  ^""^  puliation  in  a  case  of  patient 
™,  ,       ,  .  ii  ■  (M.  F.)  with  aneurism  of  the  abdominal  aorta. 

Ihe  pulse  became  stronger;  the  maxi- 
mal blood-pressure  rose  to    120   mm. 

Hg.  However,  his  kidneys  absolutely  ceased  secreting.  He  did  not  void  at  all  spon- 
taneously, and  50  c.c.  of  clear  reddish  liquid,  of  neutral  reaction  and  with  a  specific 
gravity  of  1030,  was  all  that  could  be  obtained  on  catheterization  on  the  evening  of 
Jan.  24.  It  contained  a  large  amount  of  albumen,  no  sugar,  no  casts,  a  few  red  blood- 
corpuscles,  and  a  large  number  of  pus-cells.  This  was  the  last  urine  obtainable,  even  by 
catheter. 

From  this  time  on  the  patient's  condition  became  worse.  He  complained  of 
sudden  shocks  like  electric  shocks  through  his  nervous  system,  to  which  he  responded 
by  sudden  single  twitches.  He  had  no  general  convulsions.  His  mind  remained 
perfectly  clear,  his  pulse  good  until  the  morning  of  Jan.  26  (five  days  after  the  rupture), 
when  his  pulse  gradually  became  weaker,  he  lapsed  into  unconsciousness,  and  died  at 
10.30  p.  M. 

Autopsy  confirmed  the  clinical  diagnosis,  showing  a  large  saccular 
aneurism  of  the  abdominal  aorta  which  had  ruptured  into  the  retroperi- 
toneal tissue  and  lesser  peritoneal  cavity,  causing  infarction  of  the  left  kidney  and  oblitera- 
tion of  the  vessels  to  the  right.  There  was  thrombosis  of  all  renal  vessels  and  a  tremendous 
hemorrhage  into  the  greater  peritoneal  cavity  as  well.  This  rupture  had  evidently  occurred 
at  the  time  of  the  collapse  on  Jan.  22.  There  was  an  island  of  clot  within  the  coil 
of  silver  wire  within  the  sac,  but  a  wide  free  blood  channel  between  this  clot 
and  the  aneurismal  wall,  so  that  the  clot  had  not  strengthened  the  latter 
in   the   least. 

It  is  probable  that  during  the  months  following  the  wiring,  while  he  was  free  from 
pain,  the  clot  filled  the  entire  aneurismal  sac,  and  that  the  eddy  currents  dissected  it  free 
from  the  aneurismal  wall  about  the  time  that  the  pains  returned. 
35 


546  DISEASES   OF   THE   HEART    AND    AORTA. 


DIAGNOSIS. 

The  diagnosis  of  thoracic  aneurism  is,  as  a  rule,  easy,  especially  with 
the  aid  of  the  X-ray.  Most  of  the  conditions  with  which  it  can  be  confused 
have  been  mentioned  above.  The  most  important  of  these  are  simple 
dilatation  of  the  aorta,  mediastinal  tumors,  pulsating  empyema  or  encapsu- 
lated pericarditis,  and  enlarged  mediastinal  or  branchial  glands.  Any  of 
these  may  cause  the  dulness,  the  tracheal  tug,  the  inequality  of  pupils 
and  pulse.  The  systolic  thrill  and  murmur  may  also  be  communicated  by 
a  very  solid  tumor  or  may  arise  in  a  very  vascular  sarcoma,  aberrant  thy- 
roid with  stroma,  or  metastasis  from 
I     \«  a  medullary  carcinoma  or  hyperne- 

h     %^  phroma.  A  diastolic  shock  is  scarcely 

/^,     I  \  ever  felt  over  even  the  most  vascu- 

^— — >B^^^^^^       Siv  \^  lar   tumors,  but  is,  of  course,  well 

>^       • ^^^'-v:^l>,  SwJV        marked  over   a  dilated   aorta.     The 

j^  ,  ^  -   -^   \  \    r  presence  of  a  forcible   expansile 

^  ^JjjjT^^^  ~~~^^Mi'^  pulsation  in  the  interspaces  is  suffi- 

Vif  -v/J/H^^—        "  '^^Ba'^  cient  to  exclude  tumors;  but  in  the 

Fig.  313.— Tortuous  subclavian  artery,  simu-     first    and   secoud   interspaces   when 

lating  a  small  aneurism.      The  tumor  which  it       ^liere    is    nO    aCtual     bulging    it     may 
formed    above  the  clavicle  is   indicaten    by  the  ,         i        ti  •  , 

shading.  be  due  to  a  simple  dilatation  of  the 

aorta.  The  tracheal  tug  may  further 
be  due  simply  to  displacement  of  the  heart  or  aortic  arch  or  to  enterop- 
tosis,  while  the  inequality  of  the  pulse  may  arise  from  the  presence  of  adhe- 
sions or  arteriosclerotic  plaques  about  the  origin  of  the  subclavian  arteries. 

The  absolute  diagnosis  can  almost  always  be  made  by  X-ray  exam- 
ination, but  even  then  a  tumor  may  be  encountered  whose  shadow  shows 
no  expansile  pulsation  and  whose  nature  remains  in  doubt.  The  homogene- 
ous shadow,  with  its  regular  spherical  or  oval  form  and  its  connection 
with  the  aorta,  is  usually  evidence  of  aneurismal  nature. 

In  doubtful  cases  the  greatest  care  is  necessary,  for  the  physician  should 
always  bear  in  mind  that  the  earher  the  aneurism  can  be  treated  the  greater 
the  chance  of  cure,  and  this  stage  of  hope  is  usually  the  stage  in  which  the 
physical  signs  are  still  far  from  definite. 

Occasionally  a  tortuous  carotid  or  subclavian  artery  presenting  its 
convexity  in  the  supraclavicular  fossa  may  simulate  an  aneurism,  so  that, 
as  in  the  case  seen  in  Fig.  313,  it  is  necessary  to  outline  the  supposed  aneu- 
rism with  the  tip  of  the  little  finger.  In  this  case,  which  had  once  been 
diagnosed  aneurism,  it  was  possible  to  reach  below  the  convexity  and  to 
feel  the  outline  of  a  narrow  but  tortuous  subclavian  artery.  Of  course, 
the  X-ray  examination  in  such  a  case  would  at  once  clear  up  the  diagnosis, 
even  if  the  outline  of  the  artery  could  not  be  felt. 

Another  condition  which  may  simulate  aneurism  of  the  subclavian 
artery  is  a  dilated  jugular  bulb,  which  appears  as  a  pulsating  sac  above  the 
clavicle.  This  is  especially  marked  when  tricuspid  insufficiency  is  present. 
In  such  cases  the  arterial  blood-pressure  may  be  low  and  the  arterial  pulses 
weak;  nevertheless,  the  pulsation  is  so  feeble  and  the  connection  with  the 
dilated  veins  so  evident  that  it  should  never  be  mistaken  for  an  aneurism. 


ANEURISM. 


547 


DISSECTING  ANEURISM. 

Shakelton  in  1822  gave  the  first  descriptions  of  dissecting  aneurisms, 
which  were  soon  confirmed  by  Hope  (1833)  and  Henderson  (1843).  In 
this  condition  the  coats  of  the  aorta  are  spht  longitudinally  into  two  sleeves, 
— an  outer,  originally  formed  by  the  adventitia,  and  later  lined  by  new- 
formed  intimal  endothelium;  and  an  inner  sleeve  representing  the  original 
tube  of  the  aorta,  composed  of  the  original  intima  and  media,  and  later 
also  covered  with  new-formed  endothelium. 

PATHOLOGY. 

The  condition  is  not  an  extremely  rare  one,  so  that  Bostroem  in  1887 
was  able  to  collect  reports  of  177  cases.  It  usually  arises  in  the  aorta, 
especially  at  the  beginning  of  the  descending  arch,  and  not  infrequently 
is  formed  as  the  continuation  of  a  simple  aneurism  of  the  arch.  From 
this  region  it  commonly  extends  along  the  whole  length  of  the  aorta  to 


Fig.  314. — Dissecting  aneurisms.  A.  Specimen  of  a  dissecting  aneurism  (partial  clot  formation) 
in  a  man  with  only  two  aortic  cusps.  (From  the  Arjny  Medical  Museum,  Washington,  D.  C.)  B.  Dis- 
secting aneurism  of  L.  R.,  involving  the  arch  and  the  descending  aorta.  (After  MacCallum;  kindness 
of  the  Johns  Hopkins  Hospital  Bulletin.) 


the  bifurcation,  the  arteries  sometimes  arising  from  the  inner,  sometimes 
from  the  outer  tube.  Occasionally  the  split  occurs  between  the  layers  of 
the  media,  so  that  both  sleeves  have  a  wall  of  media.  Very  infrequently 
the  outer  tube  ruptures  into  the  inner  tube  near  its  lower  end,  so  that  the 
blood  passes  back  into  the  latter. 

The  most  satisfactory  explanation  for  this  remarkable  lesion  seems 
to  be  the  following  (v.  Moller,  Flockemann,  Schede) :  As  long  as  the  lumen 
of  the  artery  is  uniform,  the  blood  exerts  only  a  lateral  pressure  upon  the 


548  DISEASES   OF   THE   HEART    AND    AORTA. 

arterial  walls,  which  acts  "  across  the  grain  "  of  the  arterial  coats.  However, 
when  calcified  plaques  project  into  the  lumen,  these  tend  to  impede  the 
blood-current  so  that  the  longitudinal  pressure  of  the  latter  acts  as  well. 
As  Bostroem  has  shown,  the  resultant  force  acts  in  a  parabola  pointing 
outward  and  downward.  When  this  is  acting  upon  an  area  where  the  media 
is  thinned  or  absent,  it  tends  not  only  to  split  the  coats  "with  the  grain" 
but  also  to  push  the  adventitia  outward.  The  wall  gives  way,  the  split 
lengthens,  and  the  outer  sleeve  is  formed.  Whether  or  not  the  aorta  then 
ruptures  depends  upon  the  ability  of  the  adventitia  alone  to  withstand 
the  blood-pressure. 

The  coagulation  of  the  blood  within  the  sac  depends  upon  the  formation 
of  fibrin  ferment  in  the  tissues  of  the  adventitia  and  the  rapidity  of  the 
blood-flow  within  the  new-formed  sac.  It  is  quite  frequent  for  extensive 
and  even  total  coagulation  of  the  contents  to  take  palce. 

SYMPTOMS    AND    SIGNS. 

A  considerable  proportion  of  the  cases  of  dissecting  aneurisms  give 
no  outward  manifestation  during  life  and  are  accidental  findings  at  autopsy. 
A  large  number  give  the  usual  signs  of  ordinary  aneurism,  especially  when 
they  arise  as  a  continuation  of  the  latter.  This  is  well  exemplified  by  the 
following  case,  which  was  under  the  writer's  observation  during  his  last 
admission  to  the  hospital.  (The  pathological  findings  and  clinical  notes 
are  taken  from  the  report  of  Professor  MacCallum.) 

L.  R.,  negro,  aged  30,  had  been  treated  in  the  Johns  Hopkins  Hospital  one  year 
previous  to  his  final  admission,  at  which  time  the  diagnosis  of  a  n  e  u  r  i  s  m  of  the  aorta 
had  been  made.  At  the  final  admission  the  patient  was  found  to  be  suffering  from  an 
arthritis  with  symptoms  of  general  fever,  sweating,  etc.  The  heart  was  enlarged,  dulness 
extending  13.5  cm.  to  left  and  3  cm.  to  right  of  midline.  There  was  visible  impulse  and 
heaving  in  second,  third,  fourth,  fifth,  and  sixth  interspaces,  far  out  in  first  and  second 
left  interspaces.  Heart  sounds  were  clear,  dull,  and  ringing;  second  sound  followed  by 
soft  diastolic  murmur  in  third  left  interspace,  not  heard  in  neck. 
Patient  died  in  delirium  with  high  fever. 

Autopsy  showed  general  streptococcus  septicaemia,  hemorrhagic  nephritis,  acute 
purulent  arthritis,  obhterative  pericarditis,  aneurism  of  ascending  aorta,  dissecting  aneu- 
rism of  the  descending  aorta.  The  aortic  orifice  is  not  dilated  (8  cm.  in  circumference).  A 
large  aneurismal  sac  (7  cm.  in  diameter)  lies  behind  the  pulmonary  artery;  it  extends 
upward  in  the  aorta  to  the  arch,  beyond  which  the  tube  becomes  double,  the  inner  tube 
(the  original  lumen  of  the  aorta)  having  for  its  walls  the  original  intima  plus  media, 
the  outer  tube  media  plus  new-formed  endothelium.  Numerous  trabeculse  jut  out 
transversely  into  its  lumen.  Some  of  the  intercostal  vessels  arise  from  the  new,  some  from 
the  old  lumen.  The  left  renal  artery  arises  from  the  old  lumen;  the  right  has  been  torn 
and  arises  from  the  outer.  At  the  lower  end  above  the  bifurcation  the  outer  tube  has 
ruptured  back  into  the  original  lumen. 

Another  type  is  exemplified  by  a  case  under  the  care  of  Professor 
Halsted;  also  reported  by  MacCallum. 

Patient,  aged  60,  subject  to  mental  disturbance  and  epileptiform  attacks,  complained 
on  May  28  of  inten.se  pain  over  the  whole  body,  which  he  could  not  locate.  On  May  28  his 
abdomen  was  much  distended  and  he  was  jaundiced.  There  was  pain  in  the  region  of 
the  appendix.  His  temperature  was  100°.  Leucocytes  20,000.  Exploratory  laparotomy 
showed  an  extremely  distended  colon  which  was  relieved  by  colostomy.  Patient  died 
the  next  day. 


ANEURISM.  549 

Autopsy  showed  a  dissecting  aneurism  along  the  whole  aorta,  splitting 
the  media.  The  outer  sleeve  of  the  descending  arch  perforated  into  the  posterior  mediasti- 
num, giving. rise  to  a  tremenduous  hsematoma  which  distended  that  space  down  to  the 
diaphragm.  The  rupture  had  evidently  given  rise  to  the  pain;  the  disintegration  of  red 
corpuscles  in  the  clot  had  caused  the  hsematogenous  jaundice.  Both  these  phenomena 
are  common  in  cases  of  this  type. 

ANEURISM  OF  THE  PULMONARY  ARTERY. 

Aneurisms  of  the  pulmonary  artery  are  very  rare  as  compared  with 
those  of  the  aorta.  Henschen  (1906)  has  recently  summed  up  the  reported 
cases.  In  contrast  to  aortic  aneurism,  he  finds  that  there  is  no  close  rela- 
tionship to  hard  work;  18  out  of  34  cases  (50  per  cent.)  were  in  men,  16  (47 
per  cent.)  in  women;  39  per  cent,  occurred  under  the  age  of  30  (as  com- 
pared with  18  per  cent,  of  aortic  aneurisms).  Acute  infectious  diseases 
and  lues  seem  to  be  the  main  etiological  factors.  The  ductus  arteriosus 
Botalli  was  frequently  found  open  (17.5  per  cent.),  which  would  indicate 
that  some  disturbance  during  fetal  life  or  soon  after  birth  had  been  a  pre- 
disposing factor.  Frequently  there  is  a  certain  degree  of  narrowing  of  the 
pulmonary  artery  (32  per  cent.).  In  8  cases  (20  per  cent.)  there  were  also 
marked  arteriosclerotic  changes  in  the  pulmonary  artery. 

Among  40  cases  there  were  the  following  complications:  pulmonary 
stenosis  2;  relative  pulmonary  insufficiency  5;  organic  pulmonary  insuffi- 
ciency; other  valvular  lesions  3. 

The  subjective  symptoms  are  not  pathognomonic  and  are  very  similar 
to  those  of  congenital  heart  disease;  palpitation,  dyspnoea  and  cardiac 
asthma,  constriction  of  the  chest,  cough,  often  oedema  of  the  lungs  and 
blood-tinged  expectoration,  intense  cyanosis,  cEdema,  anasarca,  ascites, 
hydrothorax.  Death  sometimes  results  suddenly  from  rupture,  sometimes 
from  intercurrent  pericarditis  and  endocarditis,  sometimes  from  diseases 
of  the  respiratory  tract. 

DIAGNOSIS. 

According  to  Henschen,  the  diagnosis  is  justified  when  the  following 
signs  are  all  present  simultaneously: 

1.  Intense  cyanosis  and  other  signs  of  stasis,  constriction,  and  bloody 

expectoration,  sometimes  sternal  pain. 

2.  Prominence  of  second  and  third  left  costal  cartilages  or  second  left 

interspace  and  well-defined  dulness  or  X-ray  shadow  in  this  area. 

3.  Pulsation  and  well-defined  thrill  and  murmur  in  second  left  inter- 

space. 

4.  Loud  superficial  rasping  systolic  murmur. 

5.  Hypertrophy  of  the  right  heart. 

6.  Absence  of  dilatation  or  hypertrophy  of  left  heart  (apex  dulness 

not  outside  the  mammillary  line). 

7.  Absence  of  other  signs  of  aortic  aneurism. 

The  X-ray  shadow  furnishes  the  most  important  aid  in  diagnosis. 
However,  the  correct  diagnosis  was  made  intra  vitam  only  once  or 
twice   in   his   40   cases. 


550  DISEASES   OF   THE   HEART    AND    AORTA. 


ANEURISM  OF  THE  ABDOMINAL  AORTA. 

Owing  to  its  frequency  (10-14  per  cent,  of  aneurisms)  and  its  surgical 
accessibility,  aneurism  of  the  abdominal  aorta  is  of  great  importance.  Owing 
to  its  exposed  situation,  trauma  is  a  more  frequent  cause  than  in  thoracic 
aneurism.  As  Sibson  has  shown,  it  is  usually  (133  out  of  171  cases)  situated 
just  below  the  diaphragm  and  above  the  coeliac  axis,  in  the  place  where  it 
gives  the  greatest  number  of  symptoms  and  is  most  inaccessible  to  operation. 

The  most  important  symptom  of  aneurism  of  the  abdominal  aorta 
is  abdominal  pain,  — epigastric  or  in  the  regions  of  kidney  and  gall- 
bladder, sometimes  in  the  flanks,  sides,  and  back.  The  pain  is  usually 
more  marked  on  one  side  than  the  other,  but  may  be  bilateral.  Until  the 
appearance  of  a  palpable  tumor  the  condition  may  be  readily  mistaken 
for  renal  calculus,  gastric  ulcer,  or  other  abdominal  di.sease,  or  for  psoas 
abscess.  The  pain  may  be  so  intense  as  to  require  morphine,  even  in  large 
doses,  though  acetanilid,  antipyrin,  aspirin,  etc.,  may  be  of  use  at  first. 
Palpitation  is  also  commonly  felt  in  the  aneurism. 

All  these  symptoms  are  common  in  neurasthenic  women  who  have 
vigorously  pulsating  abdominal  aortas,  especially  associated  with  enterop- 
tosis.  It  is  probable  that  in  this  condition  the  peritoneal  moorings  of  the 
aorta  are  rather  loose.  When  the  arterial  pressure  rises  at  systole,  the  angle 
curves  of  the  abdomnal  aorta  and  common  iliac  arteries  tend  to  straighten 
themselves  and  thus  throw  the  aorta  forward  toward  the  abdominal  wall, 
at  the  same  time  giving  a  painful  tug  upon  the  abdominal  nerves  as  they 
emerge  from  the  vertebral  column.  The  looser  the  moorings  of  the  aorta 
the  greater  its  excursion  and  the  greater  the  pull  upon  structures  other 
than  those  which  normally  hold  it.  Arteriosclerosis  of  the  abdominal 
vessels  may  also  give  rise  to  similar  symptoms. 

Mere  pulsation  of  the  aorta  in  the  epigastrium  and  elsewhere,  even 
when  associated  with  quite  intense  pain,  is  therefore  not  necessarily  a  sign 
of  abdominal  aneurism.  In  doubtful  cases  it  is  most  important 
to  outline  the  whole  course  of  the  aorta  by  pressing  the 
fingers  of  the  two  hands  down  on  either  side  of  the  vessel  so  as  to  include 
the  abdominal  aorta  between  them.  The  expansile  nature  of  the  pulsation 
can  be  felt  by  pressing  downward  and  inward.  Any  irregularity  or  bulging 
along  its  course  may  be  felt  readily  in  this  way.  For  the  diagnosis 
of  an  aneurism  it  is  necessary  to  outline  a  tumor  with 
expansile  pulsation  arising  from  the  abdominal  aorta,  limited  in 
extent  above  and  below,  and  spherical  or  oval  in  shape.  There  is  usually 
a  well-marked  thrill  over  an  aneurism.  The  pulse-wave  in  the  femorals  is 
usually  much  retarded  in  aneurism  (apex  beat  — femoral  pulse  interval  = 
0.24+  sec.)  but  not  in  simple  aortic  pulsation.  The  early  diagnosis  may 
sometimes  be  made  with  the  fluoroscope,  care  being  taken  to  empty  the 
bowels  by  a  day  or  two  free  purgation  and  preliminary  milk  diet,  and  then 
to  examine  the  abdomen  with  a  "compression  diaphragm"  (Kompres- 
sionsblende)  so  as  to  push  the  other  structures  aside.  Oblique  illumina- 
tions and  inflation  of  stomach  and  colon  with  air  may  be  helpful. 

As  the  aneurism  grows  it  may  press  upon  the  renal  arteries  and  veins 
and  may  cause  albuminuria,  cylindruria,  hematuria,  or  even  anuria 


ANEURISM.  551 

and  death  from  this  cause.  It  may  press  upon  the  intestines  and  cause 
intestinal  paralysis,  with  death  from  obstruction,  or  may  give 
rise  to  many  symptoms  from  pressure.  Erosion  of  the  vertebrae 
and  pressure  on  the  cord  or  cauda  equina  may  lead  to  paraplegia 
(flaccid)  and  may  cause  most  intense  pain. 

Abdominal  aneurisms  may  rupture  the  retroperitoneal  tissue  into 
the  peritoneum,  especially  the  lesser  peritoneal  sac  into  the  stomach, 
intestines,  or  vena  cava.  They  rupture  externally  in  the  epigastrium.  The 
rupture  is  attended  with  excruciating  pain  and  often  collapse,  but  death 
may  not  ensue  for  some  time  thereafter,  as  the  clotting  of  blood  in  a  small 
space  may  prevent  further  outflow  from  the  vessels.  Thus,  in  the  case 
cited  below,  the  aneurism  ruptured  into  the  retroperitoneal  tissue,  com- 
pressing the  renal  vessels.  The  pain  accompanying  and  following  rupture 
was  excruciating,  probably  owing  to  stretching  of  the  solar  plexus. 

PROGNOSIS  AND  TREATMENT  OF  ANEURISM. 

In  spite  of  the  fact  that  aneurisms  occasionally  cease  to  develop  or 
even  undergo  spontaneous  cure  by  thrombosis,  this  procedure  is  to  be  re- 
garded as  a  rarity,  and  it  is  not,  under  any  circumstances,  to  be  expected. 
By  far  the  greater  number  of  aneurisms  cause  the  death  of  the  patient 
within  from  one  to  five  years,  though  occasionally  they  remain  stationary 
for  twenty-five  or  thirt5^  It  is,  therefore,  necessary  to  attempt  to  modify 
the  course  by  treatment.  As  the  intrathoracic  aneurisms  were  not  well 
known  to  the  ancients,  their  therapy  for  aneurism  was  confined  to  ligature 
of  the  peripheral  arteries. 

Valsalva  (1666-1723)  recommended  lessening  the  force  of  the  heart- 
beat by  absolute  rest  in  the  recumbent  posture,  "starvation  diet,"  and 
frequent  removal  of  small  quantities  of  blood  by  venesection.  The  two 
former  procedures  were  revived  by  Tufnell  in  1874.  Tufnell  reported  a 
number  of  cases,  especially  of  aneurism  of  the  abdominal  aorta,  cured  by 
restriction  of  the  daily  intake  to  ten  ounces  of  solids  and  ten  ounces  of 
liquids  for  several  weeks. 

•p      ,  f  f  Bread  and  butter 60  Gm.  (oii) 

areaKtast j  j^^jj. g^  ^^    ^^jj^ 

-P^.  (  Meat 60-100  Gm.  (oii-iii) 

^^""^'' I  Milk 75-125  c.c.  (3iii-iv) 

„  (Bread 60  Gm.  (gii) 

^"PP^'" iMilk 60c.c.(3ii) 

The  patient  is  given  no  water,  and  is  not  allowed  to  rise  from  the  horizontal  position 
even  for  an  instant.  As  a  result  of  this  the  blood-pressure  falls  and  the  pulse-rate  also. 
In  his  first  case  the  pulse-rate  fell  from  104  to  69  per  minute,  equalling  a  diminution 
of  50,400  beats  in  twenty-four  hours.  The  wall  of  the  aneurism  is  spared  just  this  amount 
of  strain,  the  volume  of  blood  diminishes,  and  the  aneurismal  sac  may  gradually  contract 
down,  facilitating  clotting. 

Tufnell's  results  (cure  of  two  abdominal  and  one  popliteal  aneurism) 
are  rather  striking,  but  the  treatment  imposes  the  greatest  hardship  on 
the  patient  and  few  have  the  hardihood  to  give  it  an  adequate  trial.  That 
the  restriction  of  fluid  to  ten  ounces  daily  may  be  harmful  is  suggested  by 


552  DISEASES   OF   THE   HEART    AND    AORTA. 

the  fact  that  his  first  case  developed  urarnia  at  the  end  of  the  treatment 
and  died  from  that  about  as  soon  as  he  would  probably  have  died  from  the 
natural  progress  of  the  aneurism. 

Alonzo  Taylor  has  made  very  careful  studies  of  the  blood  in  three  patients  under 
Tufnell  treatment,  who  were  also  receiving  potassium  iodide  1  Gm.  (gr.  xv)  and  calcium 
chloride  2  Gm.  (gr.  xxx)  daily,  and  who  were  being  bled  (250  c.c.)  every  eighteen  days. 
He  found  no  change  in  the  concentration  of  the  blood  or  in  calcium  in  the  blood,  and  only 
slight  fall  of  red  corpuscles.  The  coagulation  time  was  unchanged  in  one  patient,  slightly 
shortened  in  another.  The  aneurisms  became  somewhat  smaller,  but  no  cures  resulted. 
At  the  Johns  Hopkins  Hospital  the  method  was  tried  very  assiduously  for  many  years, 
supplemented  by  subcutaneous  gelatin  injections  as  suggested  by  Lancereaux.  Later 
calcium  lactate  has  been  used.  There  have  been  but  few  satisfactory  results  (Futcher), 
though  Professor  Osier  stated  that  he  had  seen  several  cases  of  cure  in  his  extensive 
experience. 

Potassium  iodide  was  used  in  aneurism  by  Bouillaud  (1859) 
and  Chuckerbutty  (1862),  and  especially  by  Balfour,  who  found  that  it 
caused  great  relief  from  the  pain,  and  claimed  that  the  aneurism  also  dimin- 
ished considerably  in  size.  Subsequent  experience  demonstrates  the  cor- 
rectness of  the  claim  that  aneurismal  pains  are  often  relieved  b}''  potassium 
iodide,  but  few,  if  any,  cures  of  well-defined  thoracic  aneurisms  can  be  ob- 
tained by  its  use.  Its  modus  operandi  is  still  obscure,  but  it  may  cause  a 
retrogression  of  the  luetic  mesarteritis  which  is  so  often  present.  Gibson 
thinks  that  "we  may  admit  it  to  be  extremely  probable  that  under  the 
influence  of  iodide  of  potassium  ths  nutrition  of  the  walls  of  the  sac,  as 
well  as  of  the  whole  of  the  arterial  system,  undergoes  improvement." 

Wiring. — The  reason  that  an  increased  coagulability  of  the  blood 
and  a  slowed  circulation  do  not  of  themselves  produce  intrasaccular  clot- 
ting is  that  the  latter,  like  the  vessels,  is  lined  with  endothelium  and  does 
not  furnish  fibrin  ferment.  As  stated  by  Moore  in  1864,  "the  first  indis- 
pensable condition  for  the  cure  of  a  thoracic  aneurism  is  to  provide  means 
of  eUciting  fibrin  from  the  blood"  (producing  fibrin  ferment  in  situ),  and 
the  "second  ....  to  extend  the  surface  within  it  on  which  the  fibrin 
may  coagulate."  In  order  to  supplement  these  deficiencies,  Moore  sug- 
gested the  introduction  of  fine  wire  into  the  aneurismal  sac.  Murchison 
submitted  to  him  a  case  of  aneurism  of  the  ascending  aorta  which  pointed 
on  the  surface  of  the  chest.  Moore  slowly  introduced  twenty-six  yards 
of  fine  iron  wire  through  a  fine  needle.  The  pulse  fell  from  116  to  92,  the 
pulsation  of  the  tumor  almost  ceased,  but  the  patient  died  in  collapse  two 
days  later. 

Previously  to  Moore,  Guerard  (1821),  Petrequin  (1845),  and  Ciniselh 
(1847)  induced  clotting  by  passing  weak  electric  currents  between  the  tips 
of  two  needles  introduced  into  the  sac  (galvanopuncture) .  Corradi  com- 
bined the  two  methods  by  using  the  wire  as  one  pole  of  the  battery.  As 
now  performed,  the  wire  (silver  alloy)  is  attached  to  one  pole  of  the  battery. 
It  is  introduced  through  a  needle  which  is  covered  with  lacquer  to  prevent 
stimulation  of  the  intercostal  muscles,  etc.,  and  a  weak  current  (10  milli- 
amperes)  is  passed  through  it.  This  accelerates  clotting  and  gives  a 
firmer  clot. 

The  details  of  technic,  as  well  as  an  excellent  report  of  the  Hterature, 
are  given  by  Hunner.    Hunner  cites  14  cases  treated  by  wire  alone  (Moore's 


ANEURISM. 


553 


method),  with  cure  in  2  cases  of  abdominal  aneurism  (Morse  and  Langton)  ; 
with  the  combined  (wire  plus  electricity)  method  (Moore-Corradi) ,  23 
cases — 17  thoracic,  with  3  cures  (17.7  per  cent.)  (Dr.  Rosenstirn  informs 
the  writer  that  his  patient  is  still  alive  and  well  twenty  years  after  the 
operation),  and  6  abdominal  aneurisms.  Finney's  case,  who  was  appar- 
ently cured  in  1900,  died  in  1903  of  rupture  of  the  aneurism  after  intense 
suffering  for  several  years. 

Unfortunately,  the  number  of  cases  in  which  the  Moore-Corradi 
method  can  succeed  is  a  limited  one.  Its  usefulness,  as  already  pointed 
out  by  Moore,  is  limited  to  sacculated  aneurisms  of  the  aorta  and  to  aneu- 


Fin.  315. — Diagram  showing  the  various  methods  for  the  operative  treatment  of  aneurism.  Arrows 
indicate  direction  of  the  blood  stream.  A.  Ligature  above  and  below  the  sac  (Antyllus).  B.  Ligature 
above  and  below  the  sac;  removal  of  the  sac  (Hueter).  C.  Ligature  above  and  at  some  distance  from 
the  sac  (Hunter).  V.  V.  represent  vasa  vasorum.  D.  Ligature  below  the  sac  (Brasdor,  Wardrop). 
E.  Metal  band  (Halsted).  F.  Obliteration  of  the  sac  (Matas).  a,  laying  the  sutures  in  the  sac;  6,  arterial 
tube  left  patent  after  tightening  sutures;  c,  entire  lumen  obliterated  by  sutures.  G.  Successful  wiring  of 
a  sacculated  aneurism  by  the  Moore-Corradi  method,  showing  the  electrodes  (  +  ,  —  )  in  place.  H.  Wiring 
of  an  aneurism  with  wide  mouth,  showing  the  action  of  eddy  currents  in  penetrating  between  the  clot 
and  the  aneurism  wall.     (Compare  with  Fig.  316.) 


risms  of  arteries  which  have  already  been  ligated  below  the  aneurism  (Bras- 
dor's  ligature, — e.g.,  wiring  of  an  innominate  aneurism  after  ligature  of 
the  right  carotid  and  right  subclavian  arteries),  so  as  to  convert  them  into 
bUnd  sacs. 

The  narrower  the  opening  of  the  sac  the  greater  the  chance  of  per- 
manent cure,  for  the  clot  then  completely  fills  the  sac  and  the  blood  passes 
by  it  without  entering  the  old  sac.  However,  if  the  sacculation  has  a  wide 
mouth  the  condition  is  different.  The  whole  sac  may  be  filled  by  clot  at 
the  time  of  operation^,  but  the  irregularities  about  the  edges  of  the  clot 
give  rise  to  eddy  currents  which  gradually  dissect  the  clot  loose  from  the 
aneurismal  wall,  and  leave  as  an  end  result  an  unaltered  aneurism  with  an 
island  of  wire  containing  clot  floating  in  the  centre  (Figs.  315,  H,  and  316). 
In  an  individual  case  the  treatment  will,  of  course,  be  more  likely  to  succeed 
if  preceded  by  a  prolonged  period  of  absolute  rest,  restricted  diet  and  liquids, 


554 


DISEASES   OF   THE    HEART    AND    AORTA. 


WIRE 


CLOT 


and  vigorous  use  of  potassium  iodide,  so  that  the  blood-pressure  may  be 
as  low,  the  size  of  the  sac  as  small,  and  its  neck  as  narrow  as  possible.  The 
same  treatment  should  follow  the  operation  to  give  a  chance  for  the  most 
compact  adhesion  of  the  clot  to  the  aneurismal  wall. 

In  fusiform  aneurisms  the  wiring  method  is  worse  than  useless,  since 
it  merely  gives  rise  to  a  clot  in  mid-blood  stream  from  which  emboli  are 
readily  dislodged. 

Compression.  —  Aneurisms  of  the  peripheral  arteries,  and  especially 
of  the  abdominal  aorta,  are  sometimes  cured  by  compressing  that  vessel 
above  the  aneurism.    This  was  done  successfully  by  Murray  in  1864,  who 

obliterated  the  aneurism  and 
the  femoral  pulse  by  means  of 
a  tourniquet  wound  around 
the  body  above  the  tumor.  A 
number  of  similar  successful 
cases  have  been  reported  since 
Murray's,  especially  when  the 
aorta  is  compressed  with  the 
fingers.  The  operator  cannot 
continue  digital  compression 
longer  than  five  or  ten  min- 
utes at  a  time,  so  that  it  is 
often  the  custom  to  obtain 
the  assistance  of  a  whole 
class      of      medical     students 

Fig.  316. —  Specimen  of  wired  abdominal  aneurism,       W'Orking     in      relays.         In     this 
showing  an  island  of  clot  within   the  coils  of  wire  sur-  ni         i  i  i      j  i  i 

rounded  by  a  free  blood-channel.  Way  Shepherd  and  others  have 

been  able  to  keep  the  aorta 
occluded  for  twenty-four  hours,  and  have  brought  about  recovery. 

On  the  other  hand,  the  prolonged  pressure  may  bring  about  necrosis 
of  the  abdominal  wall,  intestine  and  pancreas,  or  secondary  peritonitis, 
and  intestinal  obstruction  may  result  (Bryant,  Lunn  and  Benham,  Moxon 
and  Durham).  The  method  is  therefore  still  a  daring  one,  and  is  probably 
more  severe  and  less  certain  than  Halsted's  metal  band  method.  Moreover, 
Sibson  found  133  out  of  177  abdominal  aneurisms  (75  per  cent.)  above 
the  level  of  the  cceliac  axis  where  they  could  not  be  reached  by  pressure. 

Ligature  and  Partial  Occlusion. — Double  Ligature. — The  oldest  method 
of  treating  aneurisms  of  the  peripheral  arteries  is  to  ligate  them  above 
and  below  the  sac  (Antyllus)  (Fig.  315,  A),  after  opening  the  latter  to 
remove  the  blood.  A  more  modern  modification  of  this  method  is  that  of 
Hueter,  who  dissected  out  the  entire  sac  after  Ugating,  thus  removing  a 
large  mass  of  tissue  which  would  otherwise  become  gangrenous. 

Proximal  Ligature. — Ambroise  Pare  (sixteenth  century)  departed  from 
the  procedure  of  Antyllus  by  merely  ligating  the  artery  close  above  the 
aneurism  (proximal  ligature — close  to  the  aneurism).  This  cut  off  the 
blood  supply  to  the  walls  of  the  latter  and  to  its  vicinity,  inducing  necrosis 
and  suppuration,  so  that  Anel  (1710),  Desault  (1785),  and  John  Hunter 
(1785)  were  led  to  adopt  the  proximal  ligature  at  a  considerable  distance 
above  the  aneurism  (ligature  of  brachial  for  aneurism  of  the  radial  artery; 


ANEURISM.  555 

ligation  of  femoral  below  the  adductors  for  popliteal  aneurism;  ligation  of 
femoral  above  the  adductors — in  Scarpa's  triangle — for  popliteal  aneurism) . 

Distal  Ligature. — In  the  eighteenth  century  Brasdor  and  later  Wardrop 
practised  ligation  of  the  artery  belovv-  the  aneurism  (distal  ligature)  in 
cases  like  aneurism  of  the  innominate  in  which  the  proximal  ligature  was 
impossible.  As  a  result  of  the  procedure,  a  fusiform  aneurism  of  the  innomi- 
nate becomes  practically  a  sacculated  or  flask-shaped  aneurism  of  the  aorta, 
the  innominate  artery  being  converted  into  a  blind  sac  with  narrowed 
neck,  and  coagulation  is  thus  facilitated.  This  operation  is  still  the  one 
most  commonly  performed  for  aneurisms  of  the  innominate,  carotid,  and 
first  part  of  the  subclavian  artery.  Sheen  has  collected  statistics  of  36 
cases  of  innominate  and  subclavian  aneurism,  22  before  1880  with  1  recov- 
ery, 14  after  1880  with  ,8  recoveries,  7  after  1890  with  5  recoveries  and  5 
cures.  To  this  list  might  be  added  2  cases  of  Haltsed  and  1  of  Finney 
with  recovery  and  cure.  The  deaths  before  1880  were  usually  due  to  sepsis 
and  hemorrhage.  In  operating  upon  the  innominate  artery  it  is  most  im- 
portant that  both  the  carotid  and  subclavian  arteries  should  be  ligated, 
for  if  one  of  these  arteries  be  left  open  (as  in  the  case  of  J.  B.)  the  pressure 
in  the  sac  is  increased  without  stopping  the  blood-flow  through  it,  and  the 
growth  of  the  aneurism  is  actually  favored. 

Moore  in  his  first  paper  suggested  the  combination  of  this  form  of 
ligation  with  wiring  for  aneurisms  of  the  innominate.  This  double  proced- 
ure has  not  attracted  much  attention,  as  in  the  absence  of  sepsis  the  simple 
ligature  is  often  satisfactory,  but  it  is  no  doubt  applicable  in  a  certain 
number  of  cases  where  ligation  is  not  quite  adequate. 

The  chief  objection  to  the  simple  ligation  of  arteries 
lies  in  the  fact  that  the  permanent  results  are  often  unsatisfactory,  for 
either  the  ligature  may  be  so  tight  as  to  produce  necrosis  of  the  tissues 
under  it  and  thus  bring  on  rupture  of  the  artery,  or,  as  Halsted  has  shown, 
the  arterial  lumen  may  be  re-established  in  spite  of  the  ligature.  In  many 
of  Halsted's  experiments  upon  ligating  the  larger  arteries,  the  lumen  of  the 
artery  gradually  dilated  above  and  below  the  ligature,  so  that  the  latter 
was  left  surrounded  by  a  thin  membrane  or  septum  of  scar  tissue.  This 
septum  then  perforated  in  one  or  two  places. 

Occlusion  with  Metal  Bands.  —  To  obviate  this  and  for  other  reasons 
Halsted  has  devised  a  very  ingenious  procedure,  which  consists  in  the  occlu- 
sion of  the  vessel  by  surrounding  it  with  wide  metal  bands.  These  metal 
bands  take  the  place  of  the  ligature;  but  when  properly  apphed,  do  not 
occlude  the  vasa  vasorum,  and  hence  permit  the  proper  nourishment  of  the 
arterial  wall.  Their  effect  is  more  certain  than  that  of  ligatures,  since  they 
do  not  allow  the  lumen  to  be  re-estabhshed.  The  chief  advantage,  how- 
ever, lies  in  the  ability  of  the  operator  to  obtain  a  partial  occlusion  of  the 
vessel  sufficient  to  reduce  pulsation  in  the  aneurism  to  any  desired  degree, 
without  obliterating  the  circulation  below  before  a  collateral  circulation 
has  been  established.  This  renders  it  the  operation  par  excellence  in  ab- 
dominal aneurisms  and  aneurisms  of  the  ihac  and  femoral  arteries,  in  which 
the  other  procedures  are  likely  to  be  dangerous. 

The  bands  are  made  of  No.  33  sheet  aluminum  of  a  width  varying  from  5  to  15  milH- 
metres  according  to  diameter  of  the  artery  which  is  to  be  occluded.    The  strip  is  cut  a  little 


556  DISEASES   OF   THE   HEART   AND   AORTA. 

longer  than  the  circumference  of  the  artery  (as  shown  by  a  tape  passed  around  the  artery). 
All  the  sharp  edges  must  be  carefully  filed  off  until  they  are  smooth  and  round,  lest  they 
cut  into  the  walls  of  the  artery.  The  strip  is  then  inserted  into  a  specially  devised  holder 
(Fig.  315,  E),  where  it  is  held  in  a  slot;  from  this  it  may  be  extruded  by  pressing  upon  the 
rammer  above;  and  as  it  is  extruded  below  it  is  curled  by  the  curve  at  the  foot  of  the  slot. 
The  faster  the  strip  is  extruded  the  more  tightly  it  is  curled.  The  curved  foot  of  the  holder 
is  placed  beneath  the  artery,  which  is  held  just  tightly  enough  against  the  instep  of  this 
foot  to  almost  occlude  the  lumen.  The  strip  is  extruded  by  pushing  the  rammer  just  fast 
enough  to  give  the  desired  curl.  Tension  on  the  artery  is  then  relaxed.  The  pulse  can  be 
felt  in  the  artery  below  the  band,  accompanied  by  a  well-defined  thrill.  The  band  is  then 
tightened  by  rolling  it  gently  under  the  fingers  of  one  hand  while  palpating  the  artery  below 
it  with  the  other.  The  degree  to  which  the  band  is  tightened  depends  upon  the  artery 
affected.  In  the  case  of  the  abdominal  or  descending  thoracic  aorta  it  should  be  rolled  until 
the  thrill  has  greatly  diminished  but  not  disappeared;  in  the  larger  branches  of  the  aorta 
the  pulse  may  be  made  to  disappear  absolutely.  In  a  few  minutes  a  regurgitant  pulse 
may  mark  the  appearance  of  a  collateral  circulation.  When  this  operation  is  performed 
successfully,  the  artery  becomes  gradually  occluded  at  the  point  of  constriction,  and  a 
rich  collateral  circulation  formed,  so  good  in  fact  that  in  one  case  in  which  Professor  Halsted 
had  occluded  the  descending  thoracic  aorta  Erlanger  found  the  blood-pressure  in  the  femoral 
(eight  months  afterward)  only  thirty  millimetres  below  that  in  the  brachial.  For  practical 
purposes  this  exactly  duplicates  the  conditions  in  the  adult  type  of  stenosis  of  the  isthmus 
of  the  aorta  (see  page  452),  except  that  the  anastomoses  take  place  later  and  hence  are 
not  quite  as  extensive. 

Professor  Halsted  has  now  operated  upon  a  number  of  cases  with  very- 
promising  results,  and  the  operation  gives  promise  that  in  the  hands  of  a 
surgeon  who  has  practised  the  technic,  it  may  completely  supersede  the 
methods  of  ligature  and  compression. 

Arterioirhaphy  (Matas  Operation). — R.  Matas  in  1905  introduced  an 
entirely  new  technic  in  treating  the  aneurism  of  peripheral 
arteries  exactly  in  accordance  with  the  principles  of 
treating  inguinal  herni  a — by  obliteration  of  the  sac.  The  opera- 
tion is  performed  bloodlessly. 

The  limb  is  elevated,  an  Esmarch  rubber  bandage  put  on,  or  bleeding  from  the  main 
artery  prevented  by  compression  with  a  traction  loop,  adjustable  clamps  (Crile's),  padded 
forceps,  or  digital  compression.  A  free  incision  parallel  to  the  long  axis  of  the  sac  is  then 
made  dowTi  to  the  sac  to  expose  its  whole  length.  Any  important  nerves  or  veins  should 
be  dissected  away  from  it.  The  sac  is  then  freely  opened  and  emptied. 
It  is  then  ready  for  closure.  In  most  cases  it  will  be  decided  to  obliterate  the  sac  completely, 
but  in  some  cases  of  fusiform  aneurism  it  may  be  preferable  to  leave  a  lumen  the  size  of 
the  original  artery. 

When  the  sac  is  to  be  completely  obliterated,  the  lining  of  the  sac 
is  thoroughly  scrubbed  over  its  whole  extent  with  sterile  gauze  soaked  with  salt  solution 
to  remove  the  endothelial  layer  of  the  intima,  and  thus  accelerate  union.  The  sutures 
(chromicized  gut)  are  then  applied  very  much  like  Lembert's  intestinal  sutures.  The 
most  important  point  is  to  approximate  carefully  intima  to  intima.  The  sutures 
are  laid  in  three  layers  in  such  a  way  that  the  cross-section  of  the  sac  after  suture  is  made 
to  form  a  Y;  the  first  and  deepest  layer  of  sutures  shutting  off  the  sac  from  the  artery  at 
the  Y,  and  the  third  layer  obliterating  the  cavities  in  each  arm  of  the  Y  (Fig.  315,  F). 

In  suturing  a  fusiform  aneurism  the  lumen  of  the  artery  is  preserved  by  placing  the 
first  layer  of  sutures  over  a  rubber  tube  which  is  inserted  into  the  artery.  After  the  new 
lumen  is  thus  provided  for,  the  rest  of  the  sac  is  scrubbed  and  the  sutures  laid  in  the  usual 
way.  Care  must  be  taken  to  preserve  the  blood  supply  and  nutrition  of  the  sac,  and  all 
portions  of  it  which  have  been  dissected  away  from  their  vascular  surroundings  should  be 
excised. 

In  1908  Matas  reported  the  results  of  86  such  operations,  including 
aneurisms  of  the  femoral,  the  iliofemoral,  tibial,  gluteal,  external  carotid, 


ANEURISM.  557 

axillary,  brachial,  and  subclavian  arteries,  as  well  as  the  abdominal  aorta 
(the  latter  both  fatal):  78  recoveries;  8  deaths;  4  cases  of  gangrene;  4  re- 
lapses, all  in  operations  where  the  lumen  was  restored.  In  view  of  the  fact 
that  these  86  operations  were  performed  by  fifty-two  different  operators 
the  excellent  results  obtained  are  a  striking  argument  in  favor  of  the  feasi- 
bility of  the  operation. 

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Arnold,  H.  D.:  Cause  of  Death  in  Aneurisms  of  the  Thoracic  Aorta  which  do  not  rupture; 

Report  of  five  cases.  Am.  J.  M.  Sci.,  Phila.  and  N.  Y.,  1902,  cxxiii,  72. 
Hare,  H.  A.,  and  Holder,  C.  A.:  Some  Facts  in  regard  to  Aneurism  of  the  Aorta,  ibid.,  1899, 

cxviii,  399. 
Broadbent,  W.  H.  and  J.  H.  F. :  Heart  Disease  and  Aneurysm  of  the  Aorta,  4th  edition, 

N.  Y.,  1906. 


558  DISEASES   OF   THE    HEART   AND    AORTA. 

Oliver,  W.  S.:  Physical  Diagnosis  of  Thoracic  Aneurism,  Lancet,  Lond.,  1878,  ii,  406. 

Sewall,  H.:  Some  Considerations  other  than  Aortic  Aneurism  which  determine  the  Occur- 
rence of  the  Tracheal  Tug,  Am.  J.  M.  Sci.,  Phila.  and  X.  Y.,  1901,  cxxii,  150. 

Wenckebach,  K.  F.:  Ueber  pathologische  Beziehungen  zwischen  Athmung  und  Kreislauf 
beim  Menschen,  Samml.  klin.  Vortrage  begr.  v.  R.  Volkmann,  Leipz.,  1907,  N.  F.  Inn. 
Med.,  140-141. 

Smith,  H.  L.:  A  New  Sign  in  Thoracic  Aneurysm,  Am.  Med.,  Phila.,  1902,  iii,  814. 

Fran^ois-Franck:  Recherches  cliniques  et  exp^rimentales  sur  la  valeur  comparee  des 
signes  fournis  par  I'examen  du  pouls  radial  dans  les  aneurysmes  du  tronc  brachio- 
cephalique  de  I'aorta  et  de  I'artere  sous  claviere.  Importance  du  retard  du  pouls, 
J.  de  I'anatomie  et  de  la  physiol.  norm,  et  path,  de  I'homme  at  des  anim.,  Par.,  1878, 
xiv,  113.  Recherches  sur  la  diagnostic  du  si^ge  des  aneurismes  de  I'aorta,  ibid.,  1879, 
XV,  97. 

Marey,  E.  J. :  La  circulation  du  sang  a  I'^tat  physiologique  et  dans  les  maladies,  Paris,  1881. 

V.  Ziemmsen,  A. :  Ueber  den  Pulsus  differens  und  seine  Bedeutung  bei  Erkrankungen  des 
Aortenbogens,  Deutsch.  Arch.  f.  klin.  Med.,  Leipz.,  1890,  xlvi,  288. 

Baetjer,  F.  H.:  The  X-ray  Diagnosis  of  Thoracic  Aneurysms,  Bull.  Johns  Hopkins  Hosp., 
Bait.,  1906,  xvii,  24. 

Holzknecht,  G.:  Die  Rontgenologische  Diagnostik  der  Erkrankungen  der  Brusteingeweide, 
Fortschr.  a.  d.  Geb.  d.  Rontgenstr.,  Hamb.,  1901,  Erganzungsheft,  6. 

Milanofif:  Etude  de  la  douleur  et  de  quelques  autres  symptomes  des  aneurismes  de  I'aorte 
thoracique  descendente,  Th^se,  Par.,  1900. 

Andr^f :  Contribution  a  I'^tude  des  aneurismes  de  I'aorte  descendente.  These,  Toulouse,  1904. 

Osier,  W.:  Aneurism  of  the  Descending  Thoracic  Aorta,  Internat.  Clin.,  Phila.,  1903, 
xiii  ser.,  i,  1. 

Hewlett,  A.  W.,  and  Clark,  W.  R.  P.:  The  Symptoms  of  Descending  Thoracic  Aneurism, 
Am.  J.  M.  Sc,  Phila.  and  N.  Y.,  1909,  cxxxvii,  792. 

Bostroem:  Das  geheilt*  Aneurysma  dissecans,  Deutsch.  Arch.  f.  klin.  Med.,  Leipz.,  1887, 
xlii,  1. 

Schede,  Fr.:  Zur  Aetiologie,  Verlauf,  und  Heilung  der  Aneurysma  dissecans  der  Aorta. 
Arch.  f.  path.  Anat.  u.  s.  w.,  Berl.,  1906,  cxcii,  52. 

MacCallum,  W.  G.:  Dissecting  Aneurism,  Bull.  Johns  Hopkins  Hosp.,  Bait.,  1909,  xx,  9. 

Henschen,  S.  E.:  Das  Aneurysma  Arteriae  pulmonalis,  Volkmann's  Samml.  klin.  Vortrage, 
Leipz.,  1906.  No.  422-423. 

Albertini  and  Valsalva.     Quoted  from  Gibson. 

Tufnell,  J.:  The  Successful  Treatment  of  Aneurism  by  Consolidation  of  the  Contents  of 
the  Sac,  Lond.,  1875.  The  Successful  Treatment  of  Aneurism  by  Position  and  Re- 
stricted Diet,  Trans.  Med.  Chir.  Soc.  Lond.,  1874,  Ivii,  83. 

Taylor,  A.  E.:  The  Effects  upon  the  Blood  of  the  Tufnell  Method  and  the  Calcium  Salts 
in  the  Treatment  of  Aortic  Aneurism,  J.  Exp.  Med.,  N.  Y.,  iii. 

Lancereaux  and  Paulesco:  Du  traitement  des  anevrismes  en  g^n^ral  et  de  I'anevrisme  de 
I'aorte  en  particulier  par  injections  sous-cutan^s  d'une  solution  gelatineuse.  Bull, 
de  I'Acad.  de  Med.,  Par.,  1897. 

Futcher,  T.  B.:  The  Treatment  of  Aneurismg  by  Subcutaneous  Gelatin  Injections,  J.  Am. 
M.  Asso.,  Chicago,  1900,  204. 

Bouillaud:  Gaz.  des  hop..  Par.,  1859,  61. 

Chuckerbutty:  Brit.  M.  J.,  Lond.,  1862,  ii,  61,  85.    Quoted  from  Balfour. 

Balfour,  G.  W.:  On  the  Treatment  of  Aneurism  by  Iodide  of  Potassium,  Edinb.  M.  J.,  1869, 
xiv,  33.  Further  Observations  on  the  Treatment  of  Aneurism  with  Iodide  of  Potas- 
sium, ibid.,  1870,  xv,  47. 

Moore,  C.  H. :  On  a  New  Method  of  Procuring  the  Consolidation  of  Fibrin  in  Certain  Incur- 
able Aneurisms,  Trans.  Med.  Chir.  Soc.,  Lond.,  1864,  xlvii,  129. 

Murchison,  C:  Report  of  a  Case  of  Saccular  Aneurism  of  the  Ascending  Aorta  projecting 
through  the  Anterior  Wall  of  the  Left  Side  of  the  Chest,  ibid.,  136. 

P6trequin:  Suite  et  fin  du  memoire  concemant  une  nouvelle  methode  pour  gu^rir  certains 
aneurismes  sans  operation  k  I'aide  du  galvanopuncture,  Rec.  d.  trav.  Soc.  med.  d. 
Indre-et-Loire,  Tours,  1845,  117;  also  Compt.  rend,  de  I'Acad.  d.  Sc,  Paris,  1845, 
xxi,  992. 

Ciniselli,  L.:  Osservazione  di  aneurismi  dell'  aorta  trattati  coll  elettropuntura,  Gior.  d.  r. 
Accad.  di  med.  di  Torino,  1872,  35,  xii,  418;    Gazz.  Med.  di  Milano,  1847,  vi,  9. 


ANEURISM.  559 

Hunner,  G.  L.:  Aneurism  of  the  Aorta  treated  by  Insertion  of  a  Permanent  Wire  and 
Galvanism  (Moore-Corradi  Method),  Bull.  Johns  Hopkins  Hosp.,  Bait.,  1900,  xi,  263. 

Rosenstirn,  J. :  The  Surgical  Treatment  of  a  Case  of  Aneurism  of  the  Arcus  Aortse,  wath  a 
Case  cured  by  the  Loreta-Barwell  Method,  Am.  J.  M.  Sci.,  Phila.  and  N.  Y.,  1891,  ci,  55. 

Murray,  W. :  An  Account  of  a  ('ase  of  Aneurism  of  the  Abdominal  Aorta  which  was  cured 
by  Compression  of  that  Artery  immediately  above  the  Tumor,  Trans.  Med.  Chir.  Soc. 
Lond.,  1864,  xlvii,   187. 

Shepherd,  F.  J.:  Digital  Compression  for  Aneurism,  Montreal  M.  J.,  1903,  xxxii,  70. 

Bryant,  Lunn  and  Berham,  Skerritt,  Paget.  Quoted  from  Pringle,  J.  J.:  A  Case  of  Aneu- 
rism of  the  Abdominal  Aorta  treated  by  Laparotomy  and  the  Introduction  of  Steel 
Wire  into  the  Sac,  Trans.  Med.  Chir.  Soc.  Lond.,  1887,  Ixx,  261. 

For  details  of  the  various  ligatures  see 

Lobker:  Aneurisma,  Eulenberg's  Realencycl.  d.  ges.  Heilk.,  Wien  und  Leipz.,  3d  ed.,  1894, 

i,  560,  or  Ref.  Handb.  Med.  Sc,  or  various  text-books  of  surgery. 
Sheen,  W.:  Results  of  Ligature  of  the  Innominate  Artery,  Ann.  Surg.,  Phila.,  1905,  xlii,  1. 
Halsted,  W.  S.:  Partial,  Progressive  and  Complete  Occlusion  of  the  Aorta  and  other  Large 

Arteries  in  the  Dog  by  Means  of  the  Metal  Band,  J.  Exp.  Med.,  N.  York,  1909,  xi,  373. 

The  Partial  Occlusion  of  Blood-vessels,  especially  of  the  Abdominal  Aorta,   Bull. 

Johns  Hopkins  Hosp.,  Bait.,  1905,  xvi,  346. 
Matas,  R.:  An  Operation  for  the  Radical  Cure  of  Aneurism  based  upon  Arteriorrhaphy, 

Ann.  Surg.,  Phila.,  1903,  xxxvii,  1903.     J.  Am.  M.  Asso.,  Chicago,  1906.     Statistics 

of  Endoaneurismorrhaphy,  or  the  Radical  Cure  of  Aneurism  by  Intrasaccular  Suture, 

ibid.,  1908,  H,  1667. 


PART  IV. 


I. 

PAROXYSMAL  TACHYCARDIA. 

Cotton  in  1867  described  a  peculiar  condition  in  which  attacks  of 
extreme  tachycardia  were  present,  leaving  the  heart  quite  normal  in  the 
interim.  Similar  cases  were  reported  by  Bensen,  Nothnagel,  Proebsting, 
Priesendorfer,  Pribram,  and  Bristowe,  who  considered  them  to  be  due  to 
a  sort  of  vagus  neurosis.  Bouveret,  however,  regarded  the  condition  as 
a  distinct  clinical  entity,  of  which  he  was  able  in  1889  to  collect  over 
twenty  cases  from  the  litert^ture,  and  which  he  designated  as  "essential 
(or  idiopathic)  paroxysmal  tachycardia  (tachycardie  paroxystique  essen- 
tielle)".  According  to  Bouveret,  this  condition  is  characterized  by 
attacks  in  tvhich  the  pulse  suddenly  attains  a  rapidity 
(200  to  300  per  minute)  which  is  never  seen  in  any  other  con- 
dition, even  in  the  gravest  heart  failures.  These  attacks  last  from 
several  minutes  to  several  days  or  even  weeks,  and  subside  as  sud- 
denly as  they  come.  They  sometimes  recur  for  years  and  often  for 
decades  without  seriously  interfering  with  life  and  general  health  of  the 
patient;  or,  on  the  other  hand,  an  attack  sometimes  ends  in  death. 

Bouveret's  clinical  description  was  so  complete  that,  though  many 
cases  were  subsequently  reported,  little  that  was  essential  was  added  until 
Aug.  Hoffmann  in  1900  called  attention  to  the  fact  that  the  paroxysms  of 
tachycardia  began  and  ceased  with  extreme  suddenness,  and  showed  by 
excellent  tracings  that  the  complete  change  of  rate  often  occurred  within 
the  period  of  a  single  cardiac  cycle.  Moreover,  he  showed  that  this 
change  of  rate  was  an  exact  doubling,  trebling,  or  quad- 
rupling of  the  previous  rate,  and  ended  by  halving,  quartering  or  drop- 
ping to  one-third.  For  example,  the  normal  pulse-rate  being  70,  the  rate 
during  an  attack  might  be  140,  210,  280  per  minute,  and  vice  versa.  Hoff- 
mann regarded  this  sudden  complete  change  of  rate  as 
characteristic  of  the  essential  or  idiopathic  paroxys- 
mal tachycardia,  in  contrast  to  the  simple  tachycardia 
of  exercise,  excitement,  or  convalescence,  in  which  the 
change  of  rate  is  due  to  loss  of  vagus  tone  and  comes 
on  by  a  gradual  increase  of  rate  during  a  period  of  from  one 
to  several  minutes.  Such  a  tachycardia  rarely  exceeds  120  to  140  per  min- 
ute. Even  though  it  may  give  rise  to  sharp  attacks  coming  on  more  or 
less  suddenly  and  accompanied  by  palpitation,  it  is  not  to  be  regarded 
as  idiopathic  (essential)  paroxysmal  tachycardia,  but  will  be  considered 
under  the  simple  nervous  affections  of  the  heart  (Chapter  III). 
560 


PAROXYSMAL   TACHYCARDIA. 


561 


As  will  be  seen,  one  cannot  lay  too  much  stress  upon 
the  importance  of  distinguishing  between  "paroxysms 
of  tachycardia"  and  "idiopathic  paroxysmal  tachycar- 
dia." Only  those  cases  should  be  considered  in  which  the  mode  of 
onsert  and  cessation  of  the  attack  is  carefully  given,  if  possible  with  venous 
pulse  tracings.  The  mechanism  involved  in  the  attacks  should  also  be 
noted.  It  is  only  in  this  way,  and  not  by  indiscriminate  analyses  of  cases 
in  which  the  heart  occasionally  becomes  rapid,  that  an  accurate  knowledge 
of  the  condition  can  be  acquired.  The  accurate  knowledge  of  paroxysmal 
tachycardia,  therefore,  dates  from  Hoffmann's  analysis  of  pulse  tracings. 


i^-^^-^VMA-/WWVArA~AAr  -^"^ 


Fig.  317. — Venous  pulse  in  a  case  of  paroxysmal  tachycardia  (G.  D.  R.).  (Kindness  of  the  Johns 
Hopkins  Hospital  Bulletin.)  A.  During  the  attack  (pulse-rate  144  per  minute).  Ventricular  type  of 
venous  pulse,  no  a  wave  discernible,  c,  carotid  wave.  Time  of  the  carotid  wave.  B.  Tracing  taken  five 
minute.s  later,  just  after  cessation  of  the  attack.  Pulse-rate  80.  Venous  pulse  of  the  normal  auricular 
type,  conduction  time  (a-c  interval)  normal.  C.  Tracing  from  the  same  case  taken  during  a  period  of 
irregularity  a  few  days  later,  showing  extrasystoles  with  shortened  conduction  time.  The  intervals  are 
measure*!  in  millimetres  upon  a  uniformly  running  drum. 


Still  more  accurate  knowledge  came  with  the  analysis  of  venous  tracings  as 
well,  and  of  tracings  obtained  at  the  moments  when  the  attacks  began 
and  ceased. 

Types  of  Paroxysmal  Tachycardia. — By  this  means  several  types  of 
venous  tracings  have  been  recorded: 

1.  Attacks  of  tachycardia  in  which  the  auricular  type  of  venous  pulse 
remains,  and  in  which,  at  the  cessation  of  the  attack,  the  auricles  continue 
for  a  while  at  least  at  their  old  rhythm,  the  rate  of  the  ventricles  falling  to 
half  or  less  by  the  onset  of  a  partial  auriculo(atrio)  ventricular  block  and 
a  2  : 1  rhythm  (cases  reported  by  Hoffmann,  Gerhardt,  Rihl,  and  Schmoll). 
There  may  be  periods  of  irregularity  between,  especially  just  before  and 
just  after,  attacks  due  to  the  occurrence  of  partial  block  for  occasional 
beats.  The  partial  block  even  in  these  cases  does  not  persist  indefinitely, 
but  the  rate  of  the  auricles  finally  also  becomes  slow,  and  a  1  : 1  rhythm  at 
the  slow  (normal)  rate  is  resumed. 

36 


562 


DISEASES    OF   THE    HEART    AND    AORTA. 


2.  Attacks  in  which  the  venous  pulse  is  of  the  ventricular  type  (see 
page  57)  with  no  wave  due  to  auricular  contraction,  and  which  subside  sud- 
denly with  approximate  halving  or  quartering  of  the  rate  without  signs  of 
auriculo(atrio)  ventricular  block,  the  venous  pulse  between  attacks  show- 
ing only  a  single  auricular  wave  for  each  ventricular  contraction.  Between 
attacks  there  may  be  an  irregularity  due  to  the  presence  of  extrasystoles 
with  shortened  conduction  time.  Cases  of  this  type  have  been  studied  by 
Mackenzie,  Hirschfelder,  Hay,  and  others. 

A  careful  analysis  of  the  pulse-rate  during  and  between  attacks  shows 
that  the  rate  is  by  no  means  always  a  definite  multiple,  but  varies  within 


Fig.  318. — Diagram  showing  the  various  types  of  tachycardia.  I.  Simple  non-paroxysmal  tachy- 
cardia, showing  the  gradual  increase  and  gradual  decrease  in  rate.  JUG,  venous  pulse;  A,  auricular 
impulses;  V,  ventricular  impulses;  A-V,  auriculoventricular  conduction.  II.  Paroxysmal  tachycar- 
dia, with  perristent  auricular  contraction  and  ending  in  auriculoventricular  heart-block  (2  :  1  rhythm). 
III.  Paroxysmal  tachycardia  with  auricular  fibrillation  and  ventricular  type  of  venous  pulse. 

considerable  limits  (as  for  example,  from  1.7  to  2.1  :  1;  88  to  140  and  vice 
versa  70  to  160)  even  when  tracings  are  obtained  from  the  instant  of  onset 
or  of  cessation  of  an  attack. 


OCCURRENCE    AND    ASSOCIATED    LESIONS. 

Paroxysmal  tachycardia  is  equally  common  in  both  sexes  (Bouveret, 
Hoffmann).  It  occurs  at  all  ages,  frequently  beginning  in  early  childhood 
and  persisting  for  decades.  On  the  other  hand,  it  frequently  occurs  in  old 
persons,  as  in  G.  R.  who  was  72  years  of  age.  It  is  not  usually  associated 
with  valvular  or  organic  disease  of  the  heart,  though  the  occasional  attacks 
of  sudden  tachycardias  often  seen  in  aortic  insufficiency  may  belong  to 
this  group. 

Sometimes,  as  in  the  cases  reported  by  Romberg,  there  is  associated 
coronary  sclerosis — a  group  which  seems  to  be  particularly  common.  This 
seems  to  correspond  to  the  experimental  observation  that  shortly  before 
death  the  auricles  of  the  exposed  dog's  heart  sometimes  pass  into  fibrillary 
contractions  for  a  short  period  upon  the  slightest  mechanical  irritation,  as 
well  as  to  the  experiments  of  T.  Lewis.  The  writer  has  encountered  a  num- 
ber of  cases  associated  with  mitral  stenosis. 

The  autopsy  findings  of  Mackenzie  and  Keith,  patches  of  fibrous  myo- 
carditis in  the  vicinity  of  the  His  bundle  and  coronary  sinus,  are  of  great 
interest,  but  await  further  observations  before  they  can  be  accepted  as  the 


PAROXYSMAL  TACHYCARDIA. 


563 


pathogenetic  lesion.  On  the  other  hand,  tumors,  patches  of  fibrosis,  and 
arteriosclerosis  in  the  vicinity  of  the  vagus  nucleus  in  the  medulla,  adhesions 
along  the  course  of  the  vagus  (Reinhold,  Hoffmann,  Pitres,  Oppenheimer, 
Schlesinger,  Pal),  multiple  sclerosis  (Miiller),  early  tabes  (Hirschberg)  are 
sometimes  found.  However,  S.  Hyman,  in  Sir  Victor  Horsley's  laboratory, 
has  produced  permanent  lesions  of  the  vagal  nuclei  in  a  series  of  dogs 
and  monkeys  without  ever  giving  rise  to  paroxysms  of  tachycardia. 
Nevertheless,  it  is  conceivable  that  continued  reflexes  from  irritation  of 
nerves  through  pressure  of  tumors  from  hernias,  intestinal  parasites,  etc., 
may  increase  the  irritability  of  the  heart  muscle  just  as  they  often  increase 
that  of  the  cerebral  cortex.  Indeed,  paroxysmal  tachycardia  bears  certain 
superficial  resemblances  to  a  condition  of  "epilepsy  of  the  heart,"  and  is 
occasionally  associated  with  idiopathic  epilepsy  (Nothnagel,  Schlesinger). 
In  a  number  of  cases  collected  by  Hoffmann  disturbances  of  the  digestive 
and  pelvic  organs  were   found,  in  some  cases  floating  kidney.     In  some 


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FIBRILLATION 

212, 


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--'U. 


Fig.  319. — Experimental  paroxysm  of  tachycardia  produced  by  faradization  of  tlie  dog's  auricie. 
(Ivindness  of  the  Journal  of  the  American  Medical  Association.)  ^ST  1,  2,  3,  4,  5,  faradic  stimulation  of 
the  right  auricular  appendix;  ^,  auricular  systoles;  V,  ventricular  systoles.    Time  in  seconds. 

cases  the  attacks  date  from  an  acute  cardiac  overstrain;  in  others  from 
an  attack  of  rheumatism,  with  or  without  other  cardiac  complications. 
However,  the  writer  can  confirm  the  statement  of  Hoffmann,  that  in 
many  cases  neither  the  underlying  condition  nor  the  factors  bringing 
on  the  attack  can  be  discovered. 

Onset. — The  attacks  themselves  often  occur  at  the  moment  of  awak- 
ing from  sleep,  after  or  during  defecation,  during  conditions  of  fatigue, 
and  are  sometimes  brought  on  by  nervous  excitement,  as  was  the  case  in 
the  second  attack  of  one  of  our  patients.  Mere  percussion  of  the  precordium 
has  been  known  to  bring  on  an  attack  (Bouveret).  Change  in  the  position 
of  the  body  from  the  horizontal  to  the  vertical  may  bring  on  an  attack 
(orthostatic  paroxysmal  tachycardia). 


NATURE    OF   FUNCTIONAL    DISTURBANCES. 

The  nature  of  the  functional  disturbance  is  still  obscure,  though 
several  theories  have  been  advanced.  Hoffmann,  Lommel,  Gerhardt, 
and  Mackenzie  at  first  believed  that  it  consisted  in  the  interpolation 
of  an  extrasystole  between  each  two  regular  systoles, 
calling  attention  to  the  fact  that  the  arterial  pulse  often  showed  an  alterna- 
tion of  large  and  small  beats;  but  Bayhss  and  Starling,  Hirschfelder,  and 
others  have  been  able  to  show  that  this  indicates  that  the  rate  is  a  little 


564  DISEASES   OF  THE    HEART    AND    AORTA. 

too  fast  for  the  optimum  contractions  of  the  ventricles  rather  than  that 
the  small  systoles  are  of  abnormal  origin. 

Hoffmann  (1904)  suggested  that  the  sudden  change  of  rate  (to  approxi- 
mate multiples  or  fractions  of  that  pre-existing)  represented  the  coming 
on  or  the  passing  off  of  a  block  between  the  site  at  which  the  cardiac  im- 
pulses arise  (remains  of  embryological  sinus,  the  area  bounded  by  the  venae 
cavae,  coronary  sinus,  and  septum  auriculorum  and  in  front  by  the  Eusta- 
chian valve)  and  the  auricular  muscle  tissue — a  true  sino-auricular 
block.  Just  as  in  the  cases  of  atrioventricular  block  above  mentioned, 
the  attacks  would  thus  correspond  to  the  periods  when  the  block  has  passed 
off,  the  return  to  normal  pulse  corresponding  to  the  onset  of  block.  How- 
ever alluring  this  theory  may  be,  it  must  be  admitted  that  there  is  at  pres- 
ent little  evidence  to  support  it. 

More  plausible  is  the  theory  of  Mackenzie  (1903-04),  that  these  attacks 
are  brought  about  by  a  condition  in  which  the  (Purkinje)  cells  of 
the  His  auriculo-  (atrio-)  ventricular  bundle  initiate 
the  rhythm  of  the  beat  instead  of  the  sinus.  This  theory 
is  founded  not  only  upon  the  above-mentioned  venous  tracings,  but  also 
upon  the  statement  of  Gaskell  that,  if  one  "touch  the  auriculoventricular 
ring  of  muscle  (in  the  frog)  with  the  slightest  stimulus,  immediately  a 
series  of  rhythmical  contractions  occurs,"  while  touching  the  auricular 
and  ventricular  muscle  causes  only  a  single  contraction  in  each  case.  In 
mammals,  however,  the  evidence  upon  this  point  is  very  flimsy,  for  it 
has  been  impossible  to  stimulate  the  fibres  of  the  atrioventricular  bundle 
alone  without  including  fibres  of  the  auricles  and  ventricles.  Lohmann, 
it  is  true,  stimulated  the  region  of  the  auriculoventric- 
ular bundle  (including  the  auricular  and  ventricular  muscle)  and 
obtained  simultaneous  contractions  of  the  auricles  and  ventricles,  which 
outlasted  the  period  of  stimulation.  Erlanger  has  obtained  somewhat 
similar  results,  but  does  not  regard  them  as  conclusive.  Hering  and 
Rihl  obtained  extrasystoles  with  shortened  conduction  time  and  assumed 
that  they  arose  in  the  bundle  of  His.  Mackenzie  and  Keith,  however, 
claim  to  have  found  deposits  of  cells  whose  cicatrization  "irritates  the 
bundle  and  renders  it  more  excitable  than  the  sinus.  The  contraction 
of  the  heart  then  originates  from  this  more  irritable  part.  Somewhat 
analogous  changes  follow  in  cardiosclerosis  and  in  degeneration  of  the 
coronary  arteries." 

Hi  rschf  elder ,  however,  has  been  able  to  duplicate  exactly 
the  findings  of  Lohmann  and  Hering  by  faradic  stimulation  of 
the  exposed  dog's  auricle,  not  in  the  vicinity  of  the  auriculoventricular  bundle, 
but  far  out  upon  the  auricular  appendix.  Under  these  conditions  he  ol)tained  the  follow- 
ing results:  Very  weak  faradic  stimuli  caused  the  occurrence  of  ordinary  auricular 
extrasystoles  with  normal  conduction  time,  slightly  stronger  stimuli  caused  the 
auricles  suddenly  to  assume  a  rapid  regular  rhythm  approximately >louble  the  previous 
rhythm  (the  ratio  varying  from  1.7  to  2.1  to  1).  The  ventricles  usually  followed  perfectly. 
Conduction  time  was  prolonged.  Long  continuance  or  repetition  of  this  stimulation 
or  increase  in  the  faradic  stimulus  increased  the  irritability  of  the  auricular 
muscle  (perhaps  also  that  of  the  Purkinje  fibres).  The  first  effect  was  shortening 
of  the  conduction  time.  With  still  more  increased  or  more  frequently  repeated 
stimuli  the  auricles  went  into  fibrillary  contractions  (delirium)  upon 
slight  stimulation,  the  fibrillation,  at  first  lasting  only  during  the  period  of  stimulation; 


PAROXYSMAL   TACHYCARDIA.  565 

later  or  with  stronger  stimuli,  outlasting  the  period  of  stimulus.  When  the  stimulus  and 
the  abnormal  auricular  contractions  were  only  instantaneous,  extrasystoles  with  shortened 
conduction  time  were  present  (auriculo(atrio)ventricular  extrasystoles),  just  as  in  the 
writer's  case  of  paroxysmal  tachycardia.  When  the  fibrillation  was  prolonged,  a 
long  period  of  ventricular  tachycardia  accompanied  it,  sometimes  lasting  for  many  minutes, 
and  ending  by  a  sudden  return  to  the  original  rhythm  with  nor- 
mal auricular  rate,  force,  and  normal  conduction  time.  In  the 
less  irritable  hearts  these  attacks  may  be  brought  to  a  stand- 
still by  stimulation  of  the  vagus,  but  as  irritability  increases  the  tachy- 
cardia returns.  It  is  found  that  the  whole  heart  may  be  stopped  by  vagus  stimulation, 
but  the  tachycardia  is  resumed  as  soon  as  vagus  stimulation  ceases!  Moreover,  Cushny 
and  Edmunds  who  have  investigated  paroxysmal  irregularities  with  tachycardia  in  man 
and  animals  have  found  that,  just  as  in  the  cases  of  paroxysmal  tachycardia,  the  venous 
pulse  assumes  the  ventricular  type  during  fibrillation  of  the  auricles.  This  condition  repre- 
sents the  nearest  approximation  to  paroxysmal  tachycardia  which  has  been  produced  ex- 
perimentally, and  has  led  the  writer  to  the  hypothesis  that  "  true  (idiopathic)  paroxysmal 
tachycardia  is  usually  caused  by  some  one  of  a  number  of  conditions  which  bring  about  a 
state  of  increased  irritability  of  the  heart  muscle,  especially  of  the  auricles,  which  may 
pass  into  a  state  of  fibrillation."  It  is  possible  that  cells  of  the  atrioventricular  bundle 
may  either  primarily  or  secondarily  give  rise  to  the  impulse. 


CAROTID  PRESSURE 


VOLUME  OF  VENTRICLES 

VENOUS  PRESSURE 

Fig.  320. — Diagram  showing  the  effect  of  a  paroxysm  of  tachycardia  upon  the  circulation.     The  under- 
lined portion  indicates  the  paroxysm. 

Whether  the  stimulus  originates  in  the  Purkinje  fibres  or  elsewhere 
seems  for  the  present  to  have  little  practical  importance.  More  important 
is  the  fact  that  Reid  Hunt,  Cushny  and  Edmunds,  Garrey  and  Hewlett, 
and  the  writer  have  observed  that  such  paroxysms  may  occur  not  only 
spontaneously  or  from  direct  stimulation  of  the  heart  muscle,  but  also 
upon  stimulating  the  cardiac  nerves,  either  accelerator  or  vago-sympa- 
thetic,  in  hearts  whose  irritability  is  already  abnormally  high.  Hence  it 
is  natural  that  when  the  cardiac  irritability  is  high,  small  reflex  stimuli 
bring  about  an  attack. 

Stimulation  of  Cardiac  Nerves.  —  That  something  more  than  mere 
neurogenic  influences  is  essential  was  shown  by  Gerhardt  and  Hirschfelder. 
These  observers  paralyzed  the  vagi  of  such  patients  with 
atropine  and, yet  produced  no  attack.  Hirschfelder  found 
that  slight  stimulation  of  the  accelerators,  by  exercising  his  patient  to  the 
point  of  giddiness  twenty-four  hours  after  an  attack  and  while  his  vagi 
were  paralyzed  with  atropine,  caused  a  slight  gradual  increase  of  pulse-rate, 
but  nothing  resembling  an  attack  of  paroxysmal  tachycardia.  The  con- 
dition of  extreme  irritability  of  the  cardiac  muscle  had  evidently  passed  off. 

Paroxysmal  Tachycardia  from  Coronary  Ischsemia.  —  Quite  recently  T.  Lewis 
(Paroxysmal  Tachycardia,  Heart,  Lond.,  1909,  i,  42)  has  succeeded  in  producing 
paroxysms  of  tachycardia  in  cats  and  dogs  by  ligating  one  of 
the  coronary  arteries,  especially  the  right.  These  attacks  come  on 
even  after  section  of  both  vagosympathetic  nerves,  and  hence  were  not  neuro- 
genic in   origin.     He  has  been  able  to  obtain  four  types  of  abnormal  cardiac  cycles 


566  DISEASES   OF   THE    HEART    AND    AORTA. 

during  such  paroxysms:  1.  Approximate  doubling  of  the  rates  of  both  auricles  and  ven- 
tricles, with  normal  or  slightly  diminished  conductivity;  2.  Approximate  doubling  of 
these  rates  of  these  chambers,  but  the  auricles  and  ventricles  contract  simultaneously 
(nodal  rhythm?);  3.  Fibrillation  of  the  auricles  with  approximate  doubling  of  rate  in 
the  ventricles;  4.  Approximate  doubling  of  rate  in  both  auricles  and  ventricles,  but  the 
ventricles  contract  before  the  auricles  (ventricular  tachycardia).  The  writer  has  also 
obtained  all  of  these  four  types  during  faradization  of  the  auricles,  so  that  it  would 
appear  that  they  may  all  be  traced  to  a  common  cause,  most  probably  over-excitability 
of  the  heart  muscle.  Moreover,  Rothberger  and  Winterberg  have  obtained  electrocardio- 
grams with  small  irregular  waves,  suggestive  of  auricular  fibrillation,  from  a  patient  with 
paroxysmal  tachycardia,  and  Professor  Barker,  Dr.  Bond,  and  the  writer  have  recently 
obtained  a  similar  tracing  from  a  patient  between  paroxysms,  though  electrocardiograms 
from  another  patient  in  the  midst  of  a  severe  paroxysm  showed  apparently  normal 
contractions  of  the  auricles.  Rothberger  and  Winterberg  have  obtained  exactly  similar 
electrocardiograms  from  animals  with  exposed  hearts  in  which  they  produced  a  state  of 
auricular  fibrillation  by  faradization  of  the  auricles. 

This  coronary  form  of  paroxysmal  tachycardia  is  exactly  similar  to  the  cases  of 
Romberg  and  Barker  (page  283),  but  it  is  by  no  means  certain  that  this  factor  is  tlie 
causal  one  in  all  cases  of  paroxysmal  tachycardia. 

EFFECTS    ON    CIRCULATION. 

The  effect  which  these  paroxysms  of  tachycardia  exert  upon  the  circu- 
lation is  primarily  due  to  the  deficient  filling  of  ventricles  during  the  short 
diastoles.  As  Yandell  Henderson  has  shown,  the  ventricles  fill  to  their 
normal  extent  only  when  the  pulse-rate  is  moderately  slow.  When  the 
pulse  becomes  rapid,  the  ventricles  do  not  have  time  to  fill,  and,  since  the 
period  of  systole  is  never  much  less  than  0.2  second,  it  is  evident  that  when 
the  heart-rate  is  much  above  200  the  period  during  which  filling  can  take 
place  is  very  short  and  little  blood  can  enter  the  ventricles.  The  volume 
of  the  heart  remains  small.  As  a  result  of  this  condition,  blood  stagnates 
in  auricles  and  veins,  venous  pressure  rises  (to  30  cm.  HjO  in  one  case 
examined  by  Eyster  and  Hooker),  and  with  it  there  come  engorgement  of 
the  liver  and  oedema  of  the  extremities.  Stasis  also  occurs  in  the  pulmonary 
veins,  ushering  in  oedema  and  dyspnoea,  and  sometimes  these  symptoms 
of  broken  pulmonary  compensation  dominate  the  scene  (see  page  139). 

On  the  other  hand,  the  arterial  pressure  falls,  because,  as  the  filling 
of  the  ventricle  is  small,  the  amount  which  is  driven  out  into  the  arteries 
is  diminished  correspondingly.  This  fall  in  blood-pressure  is  usually  accom- 
panied by  pallor  and  often  by  symptoms  of  cerebral  anaemia,  exactly  as 
occurs  in  hemorrhage,  surgical  shock,  or  other  conditions  in  which  the 
amount  of  blood  in  the  arteries  is  diminished.  Other  organs  also  suffer 
from  anaemia,  and  finally  also  the  heart  itself,  which  may  give  signs  of  weak- 
ening, first  evinced  by  lowered  tonus  and  dilatation.  It  is  evident  that  hearts 
whose  coronary  arteries  are  sclerotic  would  suffer  more  readily  than  those 
with  normal  blood  supply. 

PHYSIOLOGICAL   SUMMARY. 

The  pathological  physiology  of  paroxysmal  tachycardia  may  therefore 
be  summed  up  as  follows; 

Underlying   causes:     Increased  irritability  of  cardiac  muscle. 
Predisposing  factors  for  an  attack:     Slight  reflex  stim- 
ulations of  cardiac  nerves. 


PAROXYSMAL   TACHYCARDIA.  567 

Condition  during  attack:  "Doubling"  or  multiplication 
of  pulse-rate,  with  or  without  auricular  fibrillation. 

Mechanical  effects  on  the  circulation,  to  which  these 
symptoms  are  referable: 

1.  Systemic  stasis,  high  venous  pressure. 

2.  Pulmonary  stasis,  high  pressure  in  pulmonary  veins. 

3.  Anaemia  of  brain,  kidneys,  and   heart,  from  low  arterial  pressure. 

SYMPTOMS. 

Although  attacks  of  tachycardia  sometimes  run  their  course  without 
the  patient's  knowledge,  it  is  more  common  for  them  to  be  accompanied 
by  symptoms.    These  symptoms  may  be  grouped  as  follows: 

1.  Symptoms  of  cardiac  excitability. 

2.  Those  due  to  engorgement  of  systemic  veins  (failure  of  right  ven- 

tricle) . 

3.  Those   due   to  engorgement   of  pulmonary   veins   (failure   of  left 

ventricle) . 

4.  Those  due  to  cerebral  anaemia. 

1.  Palpitation,  a  feeling  of  discomfort  or  oppression  in  the  pre- 
cordium,  and  weakness  are  the  most  common  symptoms.  This  is  often 
worse  just  at  the  end  of  the  attack,  and  may,  as  in  Hay's  case,  resemble 
the  symptoms  of  angina  pectoris.  In  this  case  there  was  also  hyperaesthesia 
of  the  precordium  and  neck.  The  latter  may  be  due  to  engorgement  of 
the  cervical  veins,  as  in  angina  pectoris  it  may  be  referred  from  the  heart 
(Mackenzie). 

2.  Besides  the  above-mentioned  feeling  of  fulness  in  the 
neck,  the  patient  often  has  a  similar  feeling  in  the  abdomen  from  dis- 
tention of  the  liver,  and  swelling  of  the  feet  commonly  appears  before  the 
end  of  the  attack. 

3.  Dyspnoea  is  frequent.  It  is  striking  that  this  may  occur  with- 
out any  change  in  the  rate  of  respiration,  even  in  cases  with  severe  myo- 
cardial changes  (Romberg).  No  doubt  this  is  associated  with  engorgement 
and  high  pressure  in  the  pulmonary  veins.  It  is  often  accompanied  by 
cough  and  the  expectoration  of  mucus,  sometimes  containing  large  endo- 
thelial cells  with  blood  pigment  (Herzfehlerzellen).  Occasionally  there  is 
actual  haemoptysis  (in  three  of  Bouveret's  eleven  cases)  during  the  attack. 
Actual  pulmonary  oedema  may  indeed  set  in,  as  in  Pribram's  case, — a 
young  woman  otherwise  healthy,  whose  attacks  were  so  severe  that  "the 
pulse  became  barely  palpable.  The  patient  fell  into  a  state  of  collapse, 
and  finally  csdema  appeared  in  the  lower  part  of  the  lungs.  At  the  moment 
when  death  seemed  imminent,  when  collapse  was  at  its  height,  she  gave 
a  cry  of  anguish;  it  seemed  to  her  as  though  something  were  taken  out  of 
her  neck,  and  the  scene  suddenly  changed.  The  pulse  fell  to  76,  became 
large  and  full,  and  the  collapse  disappeared." 

On  the  other  hand,  this  sudden  change  does  not  always  occur,  and 
death  sometimes  supervenes  during  the  attack. 

The  venous  stasis  also  leads  to  albuminuria,  though  in  the  milder 
attacks  the  urine  may  be  increased  and  of  low  specific  gravity. 


568  DISEASES   OF   THE    HEART   AND    AORTA. 

4.  The  fall  in  arterial  pressure  usually  brings  about  symptoms 
of  cerebral  anaemia;  weakness,  vertigo,  and  even  extreme  nerv- 
ousness is  the  rule  during  the  attacks,  accompanied  by  restlessness,  loss 
of  appetite,  and  inability  to  sleep.  Even  syncope  may  occur.  In  a  gentle- 
man whom  the  writer  examined  some  years  ago  these  syncopal  attacks 
had  led  several  prominent  physicians  to  diagnose  Adams-Stokes  syndrome; 
when,  as  was  shown  by  the  examination  and  subsequent  observation, 
the  cerebral  anaemia  resulted  not  from  bradycardia  but  from  tachycardia. 
Fortunately,  these  attacks  have  a  tendency  to  become  milder.  Dr.  Lyon 
writes,  three  years  after  the  first  examination,  that  this  patient  "is  now 
able  to  play  cards,  go  fishing,  and  do  almost  anything  in  a  quiet  way  during 
attacks." 

PHYSICAL   SIGNS. 

Physical  signs  are  absent  between  attacks  of  par- 
oxysmal tachycardia.  During  the  attacks  the  face  is  usually 
pale,  the  expression  anxious,  the  pupils  are  equal,  the  veins  of  the  neck 
are  seen  to  be  engorged  and  often  to  show  a  positive  ''single'' 
pulsation  accompanying  each  systole  (sometimes  due  to  transitory 
tricuspid  insufficiency),  perhaps  due  to  the  feebleness  of  the  auricular  con- 
tractions. The  tumultuous  heart  action  is  often  seen  in  a  precordial  heav- 
ing and  well-marked  apex  beat.  The  area  of  cardiac  dulness  is  rarely 
increased  except  toward  the  end  of  the  attack.  It  is  u  s  u  a  1 1  y  un- 
changed or  decreased  in  size,  corresponding  to  the  diminished 
filling  of  the  ventricles.  This  diminution  in  the  size  of  the  heart 
during  an  attack  has  been  seen  with  the  fluoroscope  by  Hoffman,  Dietlen, 
and  others,  and  it  can  be  demonstrated  in  the  experimental  paroxysms. 
Towards  the  end  of  severe  attacks  dilatation  sets  in  from  cardiac  weakness. 

The  heart  sounds  may  be  unchanged,  but  usually  become  short  and 
somewhat  muffled.  There  is  often  embryocardia.  It  is  very  common  to 
hear  a  soft  systolic  over  the  right  ventricle  and  apex,  perhaps  due  to  a 
mitral  or  tricuspid  insufficiency  of  the  papillary  type. 

Sometimes  the  cardiac  rhythm  is  irregular,  owing  to  inability  of  the 
ventricles  to  follow  all  the  impulses  from  the  sinus  and  auricles  or  to  the 
presence  of  extrasystoles.  The  liver  often  is  felt  to  be  enlarged,  and  often 
shows  a  systolic  pulsation  during  attacks  (tricuspid  insufficiency),  but 
ascites  rarely  occurs.     (Edema  of  the  ankles  and  feet  is  very  frequent. 

Case  of  Pakoxtsmal  Tachtcakdia. 

G.  D.  R.,  a  hotel-keeper  aged  72,  was  admitted  to  the  Johns  Hopkins  Hospital  on 
Feb.  22,  1906,  complaining  of  palpitation  of  the  heart.  The  family  history  and  personal 
history  were  negative.  The  patient  had  always  been  a  robust  man,  had  had  no  infec- 
tious diseases  and  no  other  cardiac  manifestations. 

The  first  attack  of  palpitation  and  tachycardia  came  on  suddenly  after 
retiring  one  evening  twenty  years  before  admission.  It  caused  him  great 
fear,  but  no  pain.  The  attack  lasted  six  hours  and  left  him  weak  but  other- 
wise well.  Attacks  similar  in  character  recurred  once  a  month  until  the  winter  of 
1905-1906,  when  they  became  more  severe  and  began  to  occur  once  or  twice  a  week. 
During  the  attacks  he  passed  large  amounts  of  urine.  He  never  noticed  palpitation 
between  attacks  of  tachycardia. 


PAROXYSMAL  TACHYCARDIA.  569 

The  patient  was  a  large  well-nourished  man  of  good  color.  His  pupils  were  equal 
and  reacted  well  to  light  and  during  accommodation.  The  thorax  was  rather  barrel- 
shaped;  the  percussion  note  was  hyperresonant,  and  the  breath-sounds  were  clear,  though 
distant.  The  cardiac  impulse  was  neither  seen  nor  felt,  but  the  apex,  as  made  out  by  per- 
cussion and  auscultation,  was  situated  in  the  fifth  left  interspace  11  cm.  from  the  midhne. 
The  cardiac  dulness  extended  up  to  the  upper  border  of  the  third  rib,  but  could  not  be 
made  out  to  the  right  of  the  sternum.  The  sounds  were  distant,  but  clear.  The  pulse- 
rate  between  attacks  was  64  per  minute.  It  was  usually  regular  in  force  and  rhythm, 
of  good  volume  and  rather  high  tension;  the  blood-pressure  ranged  from  165  to  190,  the 
minimum  from  100  to  115. 

The  abdomen  was  large  and  flabby,  with  considerable  panniculus.  Liver  and 
spleen  were  not  palpable.  The  examination  was  otherwise  negative.  The  venous  pulse 
between  attacks  was  usually  normal. 

On  Feb.  23  and  March  1  and  15  the  patient  had  attacks  of  tachycardia, 
in  which  his  pulse-rate  rose  suddenly  from  80  to  88  per  minute 
to  a  height  of  144  to  160  per  minute.  The  attack  of  March  15  began  just 
after  returning  from  the  closet,  where  he  had  passed  a  soft  fluid  stool.  Tracings  made 
from  the  patient  during  this  attack  showed  what  is  probably  a  ventricular  type  of  venous 
pulse  during  the  attack.  When  the  latter  ceased,  however,  the  pulse 
resumed  the  normal  auricular  type.  There  was  no  sign  of  auriculoven- 
tricular  block.  Excitement  incident  to  being  shown  at  the  clinic  precipitated  a  second 
attack  on  March  15,  which  was  not  reUeved  by  the  application  of  an  ice-bag,  yawning, 
deep  breathing,  pressure  on  the  vagus,  in  front  of  the  sternocleidomastoid,  nor  by  admin- 
istration of  spiritus  aetheris  nitrosi,  amyl  nitrite,  or  digitalin.  The  attack  ceased  spon- 
taneously within  an  instant,  at  3.10  p.m. 

On  March  21  his  pulse  was  irregular,  due  to  the  presence  of  numerous  extra- 
systoles  with  shortened  conduction  time  (auriculoventricular?) .  These 
subsided,  however,  leaving  his  pulse  regular.  On  March  24  his  pulse  remained  at  76  in 
spite  of  the  administration  of  2mg.  atropine.  Even  rapid  walking  while  he  was  under 
the  influence  of  the  atropine  did  not  bring  on  an  attack,  nor  did  the  administration  of 
amyl  nitrite  on  March  24. 

A  very  well-defined  case  of  tricuspid  insufficiency  resulting  from  the 
cardiac  overstrain  of  a  prolonged  paroxysm  of  tachycardia  is  exemplified 
by  the  following  patient  seen  in  consultation  with  Professor  Barker. 

Case  of  Long-standing  Paroxysmal  Tachycardia. 

W.  W.  C,  clerk  in  the  U.  S.  Patent  Office,  aged  29,  had  always  been  healthy  except 
for  a  very  severe  attack  of  gonorrhoea  six  years  before  admission.  He  had  no  cardiac 
disturbance  until  seven  years  ago  (one  year  before  the  attack  of  gonorrhcsa),  when  he  had 
symptoms  of  slight  cardiac  weakness  which  was  said  to  be  valvular  ( ?),  but  these 
soon  disappeared  under  treatment,  so  that  he  was  able  to  dance  and  take  all  kinds  of  exer- 
cise without  symptoms.  Two  years  before  admission  he  awoke  one  morning, 
after  an  emission,  with  severe  palpitation  and  a  very  rapid 
weak  pulse.  He  was  kept  quiet,  an  ice-bag  put  to  his  chest,  and  he  was  given  strych- 
nine, 1.5  mg.  {jo  gr.),  also  tincture  of  strophanthus.  His  pulse-rate  dropped 
to  72.  Three  weeks  later  he  had  another  emission  and  another  attack,  and  since  then  had 
a  large  number.  The  attacks  often  come  on  after  emissions,  which  leave  him  feeling  very 
much  depressed.  They  subside  very  suddenly  and  the  pulse  returns 
to  normal  at  a  bound,  remaining  between  70  and  100  per  minute  between  attacks. 
In  the  present  attack,  however,  the  pulse-rate  has  been  rapid  continu- 
ously for  over  a  year  (since  April,  1908),  and  this  has  been  accom- 
panied by  palpitation  and  great  weakness,  occasionally  by  n  a  u  s  e  a  and  vomit- 
ing. It  has  not  been  relieved  by  strophanthin,  digitalis,  strychnine,  nitroglycerin, 
belladonna,  or  potassium  bromide. 

The  patient  is  a  pale,  nervous-looking  young  man.  The  pupils  are  rather  wide,  but 
there  are  none  of  the  ocular  signs  of  Basedow's  disease.  The  thyroid  is  not  enlarged.  There 
is  no  glandular  enlargement.  His  chest  is  long  and  rather  fiat,  but  shows  nothing  of 
importance. 


570  DISEASES   OF   THE   HEART    AND    AORTA. 

The  heart  is  much  enlarged,  the  apex  being  located  in  the  sixth  left  inter- 
space 10.5  cm.  from  the  midline.  It  is  very  movable  within  the  chest,  site  altering  5  cm. 
as  the  patient  turns  from  side  to  side.  There  is  a  heaving  impulse  over  the  precordium, 
with  systolic  retraction  of  the  interspaces  over  the  right  ventricle  and  marked  systolic 
retraction  in  the  epigastrium.  Dulness  extends  above  to  the  second  inter- 
space at  the  left  sternal  margin,  and  to  the  right  reaches  5  cm.  from  the 
midline.  Longitudinal  diameter,  20  cm.  The  area  of  flatness  extends  from  the  apex  to 
the  level  of  the  fourth  rib  and  just  b  e  yo  nd  the  sternal  margin  in  the  fifth 
right  interspace.  The  heart  sounds  are  heard  at  the  apex,  the  first  being  accom- 
panied and  followed  by  a  slight  soft  systolic  murmur  not  transmitted  to  the  axilla,  while 
the  second  is  fairly  distinct.  The  second  pulmonic  is  accentuated,  the  second  aortic  clear. 
There  are  no  diastolic  murmurs.  The  striking  feature  is  a  loud  superficial 
blowing  systolic  murmur  heard  over  an  elliptical  area  bounded 
above  by  the  level  of  the  fourth  interspace,  to  the  left  by  a 
point  9  cm.  from  the  midline,  below  by  the  middle  third  of  the 
ensiform  cartilage,  and  to  the  right  by  a  point  1  cm.  to  the  right  of 
the  sternal  margin.  This  represents  the  tricuspid  area.  The  heart's 
action  is  extremely  rapid,  about  180  per  minute,  and  is  irregular;  the  pulse  still  more  so,  as 
about  40  beats  per  minute  are  ineffectual  and  do  not  open  the  aortic  valves.  The  radial 
pulse  is  therefore  140  per  minute.  The  right  jugular  vein  is  rather  full  and  shows  a  defi- 
nite ''single''  systolic  pulsation  coincident  with  the  apex  beat.  This  is 
borne  out  by  the  tracing,  upon  which  there  are  no  waves  of  auricular  con- 
traction. The  pulse  is  small,  of  rather  low  tension,  and  very  irregular.  The  vessel 
wall  is  not  sclerotic. 

Blood-pressure  with  the  Erlanger  apparatus:  Maximal  varies  from  100  to  110 
mm.    Hg:    minimal   varies  from   70  to   80  mm. 

The  liver  is  much  enlarged  and  extends  almost  to  the  level  of  the  umbilicus. 
Its  surface  is  smooth,  the  edge  round  and  fairly  soft,  but  it  does  not  pulsate. 

His  venous  tracing  is  shown  in  Fig.  74,  page  74. 

The  patient  improved  somewhat  during  his  stay  in  the  hospital ;  but  his  pulse 
remained  rapid,  he  was  bedridden,  and  died  two  months  later. 

DIAGNOSIS. 

In  the  cases  in  which  the  pulse-rate  is  above  160  per  minute  the  diag- 
nosis rarely  presents  any  difficulty,  for  the  tachycardias  of  simple  nervous 
origin,  on  the  one  hand,  and  those  of  organic  cardiac  disease  rarely  reach 
that  height.  But  in  the  border-line  case  in  which  the  tachycardia  is  about 
140,  the  diagnosis  may  be  difficult.  The  crucial  point  in  the  differentiation 
lies  in  the  suddenness  of  the  change  of  rate,  and  for  this  it  is  important 
to  have  observed  the  beginning  and  the  end  of  an  attack,  the  sudden  rise 
to  maximum  rate  within  a  few  seconds  indicating  idiopathic  paroxysmal 
tachycardia,  while  a  gradual  step-like  or  progressive  rise  indicates  a  simple 
tachycardia.  Thus  while  the  patient  G.  R.  exemplifies  the  idiopathic  con- 
dition, the  following  case  is  typical  of  the  simple  tachycardia. 

Case  of  Simple  Emotional  Tachycardia  Resembling  Idiopathic  Paroxysmal 

Tachycardia. 

The  patient,  a  biological  student  at  the  University  of  Virginia,  aged  20  years,  had 
recovered  from  an  attack  of  typhoid  fever  about  a  year  before.  Previously  to 
this  he  had  been  strong  and  free  from  cardiac  symptoms ;  but  since  convalescence 
he  is  troubled  with  attacks  of  palpitation  and  tachycardia  in 
which  the  pulse-rate  rises  from  about  60  to  about  120  per  minute.  Slight  mental 
excitement  and  even  the  mere  mention  of  taking  a  pulse  tracing  suffices  to  bring  on 
an  attack.  Before  the  apparatus  could  be  applied  he  felt  his  pulse  begin  to  rise.  I  n  t  he 
successive   quarters   of  a   minute   the   pulse-rate   was    15,   21,   26, 


PAROXYSMAL  TACHYCARDIA.  571 

3  0  ,  having  doubled  itself  within  a  single  minute.     But  the  change   of  rate  was 
not   sudden! 

Physiological  examination  was  negative,  heart  not  being  enlarged  and  sounds  normal. 
The  case  was  therefore  considered  a  simple  tachycardia.  A  favorable  prognosis  was  given, 
which  was  verified  by  the  subsidence  of  tachycardia  and  palpitation  within  a  few  months. 

TREATMENT. 

Drugs. — As  regards  the  treatment  of  paroxysmal  tachycardia  various 
methods  have  been  employed.  The  first  essential  is  to  put  the  patient 
into  the  best  possible  physical  condition,  to  treat  any  anaemia,  digestive 
disturbance,  constipation,  disturbance  of  vision,  heaving,  enteroptosis, 
or  other  conditions  which  may  bring  about  reflex  irritations;  to  stop  the 
use  of  tea,  coffee,  tobacco,  and  alcohol,  and  so  to  arrange  the  life  of  the 
patient  as  to  do  away  with  mental  excitement,  worry,  over-exertion,  and 
fatigue.  If  necessary,  a  "rest  cure"  may  be  resorted  to.  These  measures 
may  do  much  to  diminish  the  frequency  of  the  attacks,  but  often  the  latter 
do  not  disappear  altogether.  Small  doses  of  digitalis  or  aconite  may  be 
tried  in  the  interim  between  attacks,  in  the  hope  of  keeping  them  down 
by  increasing  the  action  of  the  vagus:  or  potassium  bromide  or  valerian 
may  be  given,  in  the  hope  of  quieting  the  nervous  system ;  but  the  desired 
result  is  only  occasionally  obtained. 

To  quiet  the  attack  after  its  onset  drugs  are  of  little  avail. 
Morphine,  bromides,  etc.,  and  other  sedatives  may  diminish  the  in- 
tensity of  the  symptoms,  but  do  not  slow  the  heart-rate. 
The  administration  of  a  few  whiffs  of  chloroform,  of  amyl  nitrite,  nitro- 
glycerin, Hoffman's  anodyne,  strychnine,  digitalis  and  its  derivatives 
(digitalin,  digalen),  is  without  effect.  Though  large  doses  of  strophan- 
thin  sometimes  stop  auricular  fibrillation  in  animals,  intravenous  injection 
of  strophanthin  has  not  given  satisfactory  results  in  three  cases  of  par- 
oxysmal tachycardia  to  whom  it  has  been  administered  in  the  Johns  Hop- 
kins Hospital.  Aconite  also,  though  the  best  stimulant  for  the  vagus, 
was  without  clinical  effect  in  the  one  case  in  which  the  writer  used  it. 

The  application  of  an  ice-bag  to  the  precordium  sometimes  relieves 
the  symptoms,  but  only  rarely  is  a  sufficient  cardiac  sedative  to  stop 
an  attack. 

Mechanical  Methods  for  Stopping  the  Attacks. — A  novel  method  has  recently  been 
suggested  by  Fairbrother  based  on  experiments  upon  himself.  He  has  found  that  he  can 
cause  his  own  attacks  to  stop  by  any  sudden  or  violent  exercise  during  the  attacks, 
such  as  running,  jumping,  skipping  rope,  etc.  Needless  to  say,  these  methods,  if  resorted 
to  in  any  individual  case,  should  be  superintended  by  the  physician  and  used  with  the 
utmost  caution. 

The  paroxysms  themselves  may  sometimes  be  stopped  by  various 
mechanical  methods  which  stimulate  the  vagi;  deep  inspirations  (Noth- 
nagel),  especially  yawning,  "squeezing  arms  and  elbows  tightly  against 
the  chest  while  holding  breath  and  compressing  abdomen"  (Valsalva's 
experiment  with  elbows  compressed  against  chest)  (Hay)  ,s  wallowing, 
especially  of  ice-water,  or  belching,  may  be  successful. 

Max  Herz  has  found  it  possible  to  suppress  many  troublesome  attacks  in  his  patients 
by  bringing  about  belching  in  the  following  manner:    The  patient  is  made  to  sit  down,  fill 


572  DISEASES   OF  THE   HEART   AND    AORTA. 

his  mouth  with  water,  bend  his  head  backward  as  far  as  possible,  and  swallow.  This  not 
only  brings  about  a  desire  to  belch,  but  also  facilitates  the  eructation  of  a  large  amount  of 
gas,  and  frequently  brings  the  attack  to  a  close.  Needless  to  say,  care  should  be  taken  that 
the  belching  does  not  pass  over  into  continuous  air  swallowing  and  that  the  patient  does 
not  acquire  this  pernicious  habit  (see  page  604). 

When  belching  fails  to  stop  the  attack,  vomiting  may  be  resorted 
to,  and  frequently  proves  an  effectual  though. unpleasant  method.  Tick- 
ling the  pharynx  with  the  finger  is  usually  sufficient  to  bring  it  about, 
especially  after  swallowing  some  water.     Emetics  need  not  be  used. 

One  of  the  oldest  and  best  procedures  (Bensen,  1880)  is  pressure 
upon  the  vagus  just  to  the  left  of  the  thyroid  cartilage.  The  nerve 
which  is  just  behind  the  carotid  artery  is  pressed  very  firmly  against  the 
vertebrae  and  held  tightly  for  two  or  three  minutes.  In  a  considerable 
number  of  cases  this  stops  the  attack,  but  in  many  it  fails,  or  succeeds  for 
a  moment  and  then  the  tachycardia  is  resumed  (Priesendorfer),  just  as 
is  the  case  in  the  experimental  auricular  fibrillation. 

However,  when  the  results  of  all  methods  of  treatment  have  been  taken 
into  account,  one  is  inclined  to  share  the  feelings  expressed  by  Mackenzie 
when  he  wrote:  "In  my  early  days  I,  too,  thought  I  knew  how  to  stop 
attacks,  but  more  extended  experience  has  shown  me  that  when  they 
stopped  it  was  from  some  cause  unknown  to  me  and  which  was  independent 
of  any  means  I  employed." 

BIBLIOGRAPHY. 
Paboxtsmal  Tachycardia. 

Bouveret,  L.:  De  la  tachycardie  paroxystique  essentielle,  Rev.  de  M6d.,  Par.,  1889,  ix, 
753,  836. 

Hoffmann,  Aug.:  Die  paroxysmale  Tachycardie  (Anfalle  von  Herzjagen),  Wiesb.,  1900. 
Pathologie  und  Therapie  der  Herzneurosen,  u.s.w.,  Wiesb.,  1901.  Neue  Beobachtungen 
ueber  Herzjagen,  Deutsch.  Arch.  f.  khn.  Med.,  Leipz.,  1903,  Ixxviii,  39.  Ueber  Ver- 
doppelung  der  Herzfrequenz,  Ztschr.  f.  klin.  Med.,  Berl.,  1904,  liii,  206. 

Rihl,  J.:  Analyse  von  fiinf  Fallen  von  Ueberleitungstorungen,  Ztschr.  f.  exp.  Path.  u. 
Therap.,  Berl.,  1905,  ii.  83. 

SchmoU,  E.:  Paroxysmal  Tachycardia,  Am.  J.  M.  Sci.,  Phila.  and  N.  Y.,  1907,  cxxxiv,  662. 

Mackenzie,  J.:  On  the  Inception  of  the  Rhythm  of  the  Heart  by  the  Ventricles,  Brit.  M.  J., 
Lond.,  1904,  i,  529.  New  Methods  in  the  Study  of  Affections  of  the  Heart,  ibid.,  1905, 
i,  813.  Abnormal  Inception  of  the  Cardiac  Rhythm,  Quart.  M.  J.,  Oxford,  1907,  i, 
39.  The  Extrasystole :  A  Contribution  to  the  Functional  Pathology  of  the  Primitive 
Cardiac  Tissue,  ibid.,  1908,  i,  182  and  481.    Diseases  of  the  Heart,  Lond.,  1908. 

Hirschfelder,  A.  D.:  Observations  upon  Paroxysmal  Tachycardia,  Bull.  Johns  Hopkins 
Hosp.,  Balto.,  1906,  xvii,  337. 

Hay,  J.:  Paroxysmal  Tachycardia,  Edinb.  M.  J.,  1907,  N.  S.  xxi,  40. 

Romberg,  E.:  Lehrbuch  der  Krankheiten  des  Herzens  und  der  Blutgefasse,  Stuttg.,  1906. 
The  complete  bibliography  of  cases  will  be  found  in  the  monograph  of  Hoffmann 
and  the  articles  of  Reinhold,  Schlesinger,  and  Schmoll. 

Gerhardt,  D.:  Beitrage  zur  Lehre  von  den  Extrasystolen,  Deutsch.  Arch.  f.  klin.  Med., 
Leipz.,  1905,  Ixxxvii,  509.  Lommel,  F.:  ibid  1905,  Ixxxii,  495. 

Bayliss,  W.  M.,  and  Starling.,  E.  H.:  On  some  Points  in  the  Innervation  of  the  Mammalian 
Heart,  J.  Physiol.,  Camb.,  1892,  xiii,  407. 

Gaskell,  W.  H.:  Schaefer's  Text-book  of  Physiology,  Edinb.  and  Lond.,  1900,  ii. 

Lohmann,  A.:  Zur  Automatic  der  Briickenfasern  des  Herzens.,  Arch.  f.  Physiol.,  Leipz., 
1904,  431,  and  Suppl.,  265. 


PAROXYSMAL  TACHYCARDIA.  573 

Hering,  H.  E.,  and  Rihl,  J.:  Ueber  atrioventrikulare  Extrasystolen,  Ztschr.  f.  exp.  Path. 

u.  Therap.,  Berl.,  1906,  ii,  510.    Experimentelle  Untersuchungen  ueber  Herzunregel- 

massigkeiten  an  Affen,  ibid.,  1906,  ii,  525. 
Hirschfelder,  A.  D.:  Contributions  to  the  Study  of  Auricular  Fibrillation,  Paroxysmal 

Tachycardia,  and  the  so-called  Auriculo-  (atrio-)   ventricular  Extrasystoles,  Bull. 

Johns  Hopkins  Hosp.,  Bait.,  1908,  xix,  323. 
Cushny,  A.  R.,  and  Edmunds,  C.  W.:  Paroxysmal  Irregularity  of  the  Heart  and  Auricular 

Fibrillation,  Am.  J.  M.  Sc,  Phila.  and  N.  Y.,  1907,  cxxxiii,  66.    Studies  in  Pathology, 

Quart.  Publ.,  Aberdeen  Univ.,  1907. 
Hunt,  R.:  Direct  and  Reflex  Accelerations  of  the  Mammalian  Heart,  Am.  J.  Physiol., 

Bost.,  1899,  ii,  395. 
Garrey,  W.  E.:  Effect  of  Chemicals  on  the  Heart  Nerves,  Calif.  State  M.  J.,San  Francisco, 

1907.    Some  Effects  of  Cardiac  Nerves  upon  Ventricular  Fibrillation,  Am.  J.  Physiol., 

Bost.,  1908,  xxi,  283. 
Henderson,  Y.  (with  the  collaboration  of  M.  McR.  Scarborough  and  F.  P.  Chillingworth) : 

The  Volume  Curve  of  the  Ventricles  of  the  Mammalian  Heart,  etc..  Am.  J   Physiol., 

Bost.,  1906,  xvi,  325. 
Pribram,  A.:  Wien.  med.  Presse,  1882.     Quoted  from  Bouveret.      Lyon,  I.  P.:  Personal 

communication. 
Dietlen,  H.:  Orthodiagraphische  Beobachtungen  ueber  Veraenderungen  der  Herzgrosse 

bei  Infektionskrankheiten,  exsudativer  Perikarditis  und  paroxysmaler  Tachykardie, 

Muenchen  med.  Wchnschr.,  1908,  Iv,  2077. 
Nothnagel.     Quoted  from  Bouveret. 
Fairbrother,  H.  C.  :    A  Remedy  for  Paroxysmal  Tachycardia,  J.  Am.  M.  Asso.,  Chicago, 

1909,  liii,  300. 
Herz,  M.:  Ein  Kunstgriff  zur  Unterdriickung  der  Anfalle  von  Angina  Pectoris  und  paroxys- 
maler Tachykardie,  Wien.  klin.  Wchnschr.,  1908,  xxi,  803. 
Bensen:  Beri.  klin.  Wchnschr.,  1880. 


II. 

THYROID  HEART. 

The  cardiac  disturbances  associated  with  thyroid  disease  were  the 
most  striking  features  observed  by  Parry  in  1815  in  the  first  described  cases 
of  exophthalmic  goitre.  His  first  case  died  of  heart  failure.  Graves  (1835), 
Basedow  (1848),  Stokes  (1854),  and  Trousseau  (1856)  were  also  impressed 
by  the  cardiac  features  of  this  disease.  Trousseau  found  them  especially 
important  in  the  "formes  frusies  "  or  "  atypical "  forms  to  which  he  called 
attention,  likening  such  cases  to  a  defaced  (''fruste")  coin. 

The  important  role  which  these  "formes  frustes"  of  Basedow's' 
disease  play  in  many  cases  of  so-called  cardiac  neurasthenia  and  hysteria 
has,  since  Trousseau,  been  recognized  with  increasing  frequency,  and  espe- 
cially since  Friedrich  Kraus  in  1899  called  attention  to  them  by  introducing 
the  term  "Kropfherz"  (''goitre  heart"  or  thyroid  heart),  which  is  now 
widely  used  in  Germany. 

FORMS    OF    CARDIAC    DISTURBANCE    DUE    TO    THYROID    DISEASE. 

Strictly  speaking,  as  shown  by  Rose,  Schranz,  and  Minnich,  there  is 
some  cardiac  disturbance  with  all  forms  of  goitre.  Four  main  forms  of 
cardiac  disturbance  may  thus  be  distinguished,  due  to: 

I.  Pressure  of  the  goitre  upon  the  trachea,  bronchi,  veins,  chest, 
and  sympathetic  ganglia  (in  simple  goitre) ,  pneumo-mechanical 
goitre  heart  (Rose) . 
II.  Hypothyroidism  (in  myxcedema,  cretinism,  and  achondroplasia). 

III.  Hyperthyroidism  (exophthalmic  goitre  and  formes  frustes). 

IV.  Goitre  secondary  to  the  cardiac  disease  (goitre  cardiaque,  "car- 

diac goitre"). 

CARDIAC   DISTURBANCES   FROM   PRESSURE   OF   THE   THYROID. 

Potain  in  1863  and  Rose  in  1878  reported  cases  of  heart  failure  and 
more  or  less  sudden  death  in  cases  in  which  large  colloid  goitres  pressed 
upon  the  veins  and  trachea.    Such  a  goitre  has  several  mechanical  effects: 

1.  It  may  prevent  adequate  filling  of  the  lungs  and  thus 
produce  emphysema,  deficient  aeration  of  the  blood,  and  later  asphyxia. 
The  chronically  deficient  aeration  of  the  blood  may  lead  to  secondary  car- 
diac overstrain  and  finally  to  myocardial  weakness.  This  will  be  enhanced 
by  all  pulmonary  infections. 

'  Basedow  ("Bas-e-do").    Dock  after  a  careful  study  of  priorities  advises  the  accept- 
ance of  this  name,  which  was  the  first  unobjectionable  term  given  and  is  the  one  most  widely 
accepted. 
574 


THYROID   HEART.  575 

2.  The  goitre  often  presses  on  the  sympathetic  ganglia  on 
one  or  both  sides  of  the  neck,  thus  stimulating  the  accelerators  and  bringing 
on  a  chronic  tachycardia  just  as  is  produced  in  Basedow's  disease.  MuUer's 
muscle  in  the  orbit  may  also  be  stimulated  and  exophthalmos  produced. 
This  exophthalmos  is  often  unilateral.  The  condition  of  exoph- 
thalmos and  tachycardia  from  the  pressure  of  a  simple 
goitre    is  known  as  pseudo-Basedow's   disease.' 

Case  of  Simple  Goitre  Resembling  Basedow's  Disease. 

Such  a  case  is  represented  by  that  reported  by  Potain  in  1863 1^  M.  K.,  servant  girl, 
aged  50.  Complains  of  palpitation,  feeling  of  pressure  in  chest,  attacks  of  suffocation' 
irregular  menstruation.  She  has  had  goitre  all  her  life,  unaffected  by  iodine  treatment. 
For  some  years  her  eyes  have  been  larger  than  before.  She  has  lost  weight,  has  suffered 
from  dyspnoea  especially  on  exertion,  she  has  throbbing  of  the  goitre,  and  her  legs  are 
swollen.  Her  pulse  is  152,  irregular.  Apex  is  in  the  sixth  interspace  13  cm.  from  midline. 
There  is  heaving  of  the  entire  precordium.  At  the  apex  and  over  the  precordium  there  is 
a  meso-systolic  murmur.  The  veins  of  the  neck  are  dilated.  There  is  a  large  goitre  which 
does  not  pulsate  and  no  murmur  is  heard  over  it.  Digitalis  is  without  effect, 
and  the  patient  died  from  pulmonary  oedema  11  days  after  admission. 

Autopsy  showed  colloid  cystic  goitre  with  some  hemorrhages  from  stasis,  slight 
infarction  of  the  lungs,  and  a  somewhat  enlarged,  very  flabby  heart. 

The  livor,  orthopnoea,  asphyxia,  and  sudden  death,  as  in  Rose's  case, 
are  due  to  pressure  upon  the  air-passages,  and  are  to  be  regarded  as  cardiac 
symptoms.  The  respiratory  origin  of  this  suffocation  is  seen  in  the  very 
marked  inspiratory  (not  systolic)  retraction  of  all  the  thoracic  interspaces. 


CARDIAC   AFFECTIONS    OF   HYPOTHYROIDISM   (CARDIOPATHIA 
THYREOPRIVEA)    (KRAUS). 

In  all  the  conditions  in  which  there  is  atrophy  of  the  glandular  tissue 
of  the  thyroid  and  diminution  in  the  internal  secretion  of  the  gland,  there 
are  symptoms  of  cardiac  weakness.  The  patients  get  out  of  breath  on  very 
slight  exertion.  The  pulse  is  small  and  weak,  but  may  be  either  slow  or 
slightly  accelerated  (Kraus) .  This  is  due  to  the  fact  that  the  physiological 
vagus  tone  is  largely  due  to  the  thyroid  secretion  (v.  Cyon),  and  when  it 
is  deficient  there  is  an  overstimulation  of  the  accelerators.  However,  as 
Kraus  points  out,  the  cardiac  features  in  cachexia  thyreoprivea  are  not 
prominent  features  of  the  disease,  and  hence  are  of  little  importance  in 
connection  with  diseases  of  the  heart. 

Revilliod  has,  however,  called  attention  to  another  effect  of  hypo- 
thyroidism upon  the  circulation,  namely,  early  arteriosclerosis  with  cal- 
careous deposits.  This  effect  has  also  been  produced  by  v.  Eiselsberg  in 
new-born  lambs  from  which  he  removed  the  thyroid  glands.  In  contrast 
to  other  experimental  arteriosclerosis,  the  arterial  changes  affected  the 
intima  and  not  the  media. 

^  In  some  cases,  however,  this  is  not  due  to  pressure  on  the  sympathetic  but  to  the 
activation  of  thyreoglobulin  by  the  iodine  treatment.  Occasionally,  moreover,  a  goitre 
shows  in  one  part  colloid  degeneration,  in  another  hyperplasia  like  that  of  Basedow's  disease. 

2  Bull,  de  la  Soc.  d'Anat.  de  Paris,  1863,  p.  87,  quoted  from  Minnich. 


676 


DISEASES   OF   THE   HEART    AND    AORTA. 


DISTURBANCES   DUE   TO   HYPERTHYROIDISM. 

Basedow's  Disease  {also  "Formes  frustes,"  and  Accidental  Hyperthyroidism 
in  the  Treatment  of  Obesity). 

As  stated  above,  these  conditions  present  the  most  important  cardiac 
features  which  are  due  to  disturbed  thyroid  metabolism. 

PATHOLOGY,    PATHOGENESIS,    AND    PATHOLOGICAL    PHYSIOLOGY. 

The  veil  of  mystery  has  been  lifted  from  diseases  of  the  thyroid  by  the 
hands  of  the  physiological  chemists.  The  surgeons  Astley  Cooper,  Rever- 
din,  and  Kocher  had  found  that  extirpation  of  the  thyroid  for  goitre 
led  to  myxoedema,  and  Pisenti  Gley  and  ^'assale  had  demonstrated 
that  these  symptoms  could  be  prevented  by  feeding  the  dried  thyroid  sub- 
stance. But  the  accurate  knowledge 
dates  from  the  studies  of  Baumann 
and  his  pupils,  Roos  and  Oswald. 

Thyreoglobulin   and    lodothyrin. 

— Baumann,  Roos,  and  Oswald  have 

shown  that  the  active  principle  of  the 

thyroid  is  a  globulin  (iodothyreo- 

globulin)   which   contains    all    the 

iodine  of  the  gland.     Thyreoglobulin 

f:       A  "  ^^H      is  at   first  formed  within  the  cells 

r    ^^^^  m^^^^M      ^^^^    from    iodine     and     later 

I^^^^B  ^^^^^M      acquires   its   iodine    from   the 

^^^^^^  ^^^^^H      blood,  becoming  iodi;ccd  thyreoglob- 

1^^^^^  ^^^^^H      ulin  or  iodothyreoglobulin.    The  cells 

E      ^^B  -'^^  ^^^^^M      secrete   thyreoglobulin   more    readily 

fg"  ^B  ^^^^B      after  it  is  combined  with  iodine.     In 

•»  ^  ^^      cases  of  colloid  goitre  when  the 

blood  content  is  low  in  iodine,  the 
cells  become  loaded  with  the  iodine- 
free  thyreoglobulin  and  undergo  col- 
loid degeneration.  Iodine-free 
thyreoglobulin  is  physio- 
logically inactive,  and  the 
entire  activity  of  the  gland 
is  due  to  the  iodized  thyreoglobulin.  Indeed,  as  Baumann  has 
shown,  it  is  due  to  a  comparatively  simple  molecular  group  with  which 
the  iodine  is  combined,  and  which  can  be  split  off  from  the  rest  of 
the  globulin  molecule  by  hydrolysis  with  HjSO^  (iodothyrin). 

Effect  of  Thyreoglobulin  on  Thyroid  Structure. — According  to  Oswald, 
it  is  the  state  of  the  thyreoglobulin  which  determines  the  histological 
changes  in  the  thyroid.  When  the  iodine-free  thyreoglobulin  accumulates 
in  the  cells,  they  become  overloaded  with  colloid  and  gradually  undergo 
colloid  degeneration,  so  that  the  acini  are  found  surrounded  with  the  original 
single  layer  of  flat  epithelial  cells  in  all  stages  of  colloid  degeneration,  whose 
disintegration  adds  to  the  colloid  within  the  lymph  spaces  and  within  the 
acini.     (Oswald,  Huerthle.) 


Fia.  321.  —  Photograph  of  :i  patient  with 
Basedow's  disease.  (Kindness  of  Prof.  Blootl- 
good.) 


THYROID    HEART.  577 

An  excess  of  the  iodized  product,  on  the  other  hand,  stimulates  the 
cells  to  hyperplasia,  so  that  instead  of  a  single  layer  of  columnar  epitheUum 
the  cells  about  the  acini  are  found  to  be  several  layers  and  protrude  into 
the  lumen  in  irregular  papillary  masses  suggesting  adenomatous  changes 
(Halsted,  Oswald,  MacCallum,  Wilson).  The  same  hyperplasia  takes  place 
as  a  compensatory  process  when  a  part  of  the  gland  is  removed  (Halsted, 
Marine).  The  colloid  gradually  disappears  from  the  lumen  as  glandular 
activity  and   hyperplasia   progress  and  as   the  symptoms  become  more 


Fig.  322. — Photograph  of  a  portion  of  the  thyroid  gland  removed  from  the  patient  shown  in  Fig.  321. 

(Kindness  of  Prof.  Bloodgood.) 

severe,  and  in  very  bad  cases  it  may  be  entirely  absent  (Marine  and  Wil- 
liams, Wilson).  The  arteries  and  veins  are  very  much  dilated  (C.  Ger- 
hardt).  When  the  iodine  is  administered  in  cases  of  colloid  goitre,  the 
excess  of  thyreoglobulin  may  be  suddenly  iodized  and  by  escaping  into  the 
blood  may  give  rise  to  symptoms  of  hyperthyroidism  (palpitation  tachy- 
cardia, tremor,  loss  of  weight,  exophthalmos — Basedowification  of  a  simple 
goitre).  When  there  is  an  excess  of  iodine  and  iodized  thyreoglobulin  in 
the  blood,  the  symptoms  are  the  same  as  arise  from  the  administration 
of  thyroid  substance   (thyreoglobulin  or  iodothyrin,  its  split  product). 

PHYSIOLOGICAL    EFFECTS    OF    THYROID    SECRETION. 

It  has  been  shown  that  the  effects  of  excess  of  thyroid  secretion  in 
the  blood  are: 

1.  An  increase  in  metabolism,  especially  in  the  oxidation 
processes  and  the  breaking  down  of  proteids  in  the  tissues  and  bone, 
giving  rise  to  an  increase  in  N  and  P2O5  (Fr.  Miiller)  excreted  and  in  the 
gas  metabolism  (Magnus- Le vy) .  In  man  this  finds  its  concrete  expres- 
sion in  the  loss  of  weight,  due  especially  to  loss  of  muscle  substance  (Bau- 
mann  and  Roos). 

2.  There  is  a  general  stimulation  of  the  peripheral 
nerves  both  medullated  and  sympathetic.  Y.  Cyon,  Roos,  Oswald 
and  Kraus,  and  Friedenthal  have  shown  that  these  substances  have  several 
distinct  actions  on  the  circulation: 

37 


578 


DISEASES   OF   THE    HEART    AND    AORTA. 


A.  They  stimulate  the  depressor  or  afferent  nerves  from  the  heart,  giving  rise  on  the 
one  hand  to  the  cardiac  sensations,  palpitation,  and  anginal  pains,  and  on  the  other  hand 
to  the  vasodilation  and  low  diastolic  blood-pressure  which  are  often  observed  in  these  cases 

B.  They  stimulate  both  the  vagi  and  the  accelerator  nerves.  The  action  upon  the 
accelerators  predominates,  however,  and  tachycardia  is  thus  produced.  The  vagus  still 
remains  irritable,  however,  and  the  heart  can  be  slowed  by  pressure  on  it.  The  same 
stimulation  of  the  other  fibres  of  the  cervical  sympathetic  gives  rise  to  the  peculiar  ocular 
signs  of  Basedow's  disease  (see  page  583) . 

C.  Cleghorn  has  shown  that  thyroid  extract  has  a  direct  action  on  the  cardiac 
muscle,  increasing  the  size  and  force  of  the  contraction,  which  manifests  itself  in  the 
increased  pulse-pressure,  increased  maximal  pressure,  and  cardiac  hypertrophy. 


Fig.  323. — Drawing  of  a  histological  specimen  from  the  same  thyroid.  The  histological  picture 
of  advanced  thyroid  hypertrophy  observed  in  cases  of  Graves's  disease  in  which  the  symptoms  are  most 
marked.  (Bloodgood,  Surg.  Gyn.and  Obstcs.,  August,  1905,  vol.  i,  p.  113.)  This  drawing  was  made  in 
June,  1903. 


Biochemical  Evidences  of  Hyperthyroidism. — Falta  and  Zuelzer,  Kraus  and  Frieden- 
thal  have  shown  that  thyroid  extract  directly  antagonizes  adrenalin  in  its  pupillo-dilator 
action  on  the  frog's  eye,  and  that  this  can  be  used  as  a  test  for  hyper- 
thyroidism  in   clinical   cases. 

Another  important  biochemical  blood  test  for  hyperthyroidism  is  that  of  Reid  Hunt, 
who  has  shown  that  the  blood  of  such  patients  increases  the  resistance  of  mice  to  poisoning 
with  acetonitrile  and  morphine,  so  that  the  lethal  dose  is  thus  doubled. 

All  these  investigations  have  proved  without  doubt  that  in  Basedow's  disease  there 
is  an  excess  of  thyroid  secretion  into  the  blood  (as  claimed  by 
Mobius),  and  that  the  secretion  is  indistinguishable  from  that  of  the  normal  thyroid, 
representing  a  condition  of  hyper thyreosis  (increased  secretion)  rather  than  of 
dysthyreosis  (altered  secretion).  Whether  they  will  be  of  practical  value  in  the  diag- 
nosis of  the  puzzling  "  formes  frustes"  remains  still  to  be  determined,  since  the  excess  of 
thyreoglobulin  in  the  blood  of  these  cases  may  be  too  small  for  chemical  recognition. 


THYROID    HEART.  579 

It  is  possible  that  this  anti-adrenaUn  action  may  be  responsible  for 
the  brownish  pigmentation  (JelUnek's  sign)  which  occurs  in  many  cases 
of  hyperthyroidism,  especially  about  the  eyelids.  This  pigmentation  some- 
what resembles  the  pigmentation  of  Addison's  disease  (lack  of  adrenaUn 
secretion).  Kraus  and  Friedenthal  have  also  found  that  this  antagonistic 
action  upon  the  frog's  pupil  is  valuable  in  diagnosis,  since  it  is  given  by 
the  blood  of  patients  with  Basedow's  disease,  but  not  by  the  blood  of 
neurasthenics  and  hysterical  patients.^ 

V.  Cyon  has  shown  the  very  important  fact  that  injection  of 
thyroid  exact  or  iodothyrin  causes  an  increased  blood 
flow  through  the  thyroid  gland,  probably  thus  acting  as  a 
hormone  to  increase  its  own  secretion  and  to  introduce  a  vicious  circle: 

Hyperthyroidism 
(Basedow's  disease) 

T  i 

Increased  thyroid  Increased  blood  flow 

secretion  *~  through  thyroid 

It  is  this  increased  dilatation  of  the  arteries  which  gives  rise  to  the 
murmurs  over  the  thyroid  in  Basedow's  disease  (Guttmann). 

ETIOLOGICAL   FACTORS. 

Basedow's  disease  is  more  common  in  women  than  in  men  (805  women, 
175  men  in  Buschan's  980  cases) ;  60  per  cent,  occur  in  the  fourth  decade 
of  life  (Buschan).  In  Passler's  58  cases  there  were  4  under  15  years,  29  at 
from  15  to  25  years,  18  at  25  to  45  years,  7  over  45  years. 

Basedow's  disease  is  very  widespread,  but  is  somewhat  more  rare  in 
regions  where  simple  goitre  is  common  than  elsewhere, 
perhaps  owing  to  the  lesser  intake  of  iodine.  Heredity  plays  some  role; 
mental  and  nervous  disease,  diabetes,  and  tuberculosis  are  often  found  in 
the  same  family.  In  one  famous  family  reported  by  Osterreicher  eight 
out  of  ten  children  of  a  hysterical  woman  had  Basedow's  disease,  and  one 
of  these  daughters  had  three  children  with  the  same  illness. 

The  following  list  gives  the  predisposing  factors  in  the  series  of  A. 
Kocher  and  of  Landstrom: 

Cases. 

Gradual  onset  with  etiological  factors  unknown 28 

Pregnancy 10 

Chlorosis 7 

At  first  menstruation 6 

After  fright,  shock,  or  grief 5 

After  fatigue 8 

Infectious  diseases  (influenza  alone,  7) 13 

Old  simple  goitre 5 

Sojourn  at  high  altitude 2 

Heredity 1 

Appendicitis 1 

Total 86 

•  It  seems  doubtful  whether  the  blood  of  cases  with  mild  formes  frustes  contains 
enough  excess  of  thyreoglobulin  to  give  this  test  a  hard-and-fast  diagnostic  significance. 


580  DISEASES   OF  THE   HEART   AND    AORTA. 

It  will  be  seen  that  infectious  diseases  and  especially  influenza  con- 
stitute the  most  common  cause.  De  Quervain  has  found  a  subacute  thy- 
roiditis quite  common  in  these  conditions,  especially  in  influenza,  typhoid 
fever,  rheumatism  (as  in  Parry's  first  case),  and  diphtheria,  and  this  thy- 
roiditis was  followed  by  Basedow's  disease  within  a  few  months  in  about 
20  per  cent,  of  the  cases.  Boggs  and  Sladen  have  found  mild  thyroiditis 
present  in  most  of  the  cases  of  typhoid  fever  in  which  the  pulse  is  over 
120  at  the  height  of  the  fever.  Tonsillitis  may  also  be  a  forerunner;  and 
Engel-Reimers  has  found  acute  thyroiditis  in  secondary  lues  leading  to 
Basedow's  disease.  After  pregnancy  the  hyperthyroidism  which  is  normally 
present  in  that  condition  may  increase  and  lead  directly  into  Basedow's 
disease.  The  coexistence  of  puerperal  infection,  mastitis, 
fright,  grief,  or  shock  undoubtedly  predisposes  to  the  disease, 
as  in  the  case  of  a  girl  under  Friedrich  Miiller's  care,  whose  symptoms 
began  when  she  was  suddenly  deserted  by  her  lover  just  after  the  birth  of 
an  illegitimate  child.  In  one  of  v.  Graefe's  cases  the  symptoms  set  in  within 
a  few  days  following  a  night  of  sexual  excesses.  These  factors 
may  act  by  producing  a  reflex  dilatation  of  the  vessels  in  the  thyroid. 
Thus,  Trousseau  writes  of  a  woman  of  53  who  suffered  deep  grief  from 
the  death  of  her  father.  "  One  night,  after  she  had  been  crying  for  a  long 
time,  she  suddenly  felt  her  eyes  swell  and  lift  up  her  lids,  her  thyroid  gland 
increase  notably  in  size  and  throb  in  an  unusual  manner;  she  had  at  the 
same  time  violent  palpitation  of  the  heart."  The  writer  on  one  occasion 
had  the  opportunity  to  observe  a  case  of  acute  enlargement  of  the  thyroid 
in  a  man  of  thirty,  associated  with  tremor,  tachycardia,  palpitation,  slight 
V.  Stellwag's  but  no  other  ocular  sign.  The  disturbance  followed  the  inges- 
tion of  two  cups  of  strong  coffee  at  a  time  of  great  worry  and  was  compli- 
cated by  a  mild  attack  of  "grippe."  The  enlargement  of  the  thyroid  was 
sufficient  to  prevent  buttoning  the  collar.  It  subsided  entirely  after  24 
hours,  and  with  it  the  symptoms  of  hyperthyroidism.  It  is  probable  that 
the  grippe  (influenza  or  streptococcus  infection)  rendered  the  thyroid  par- 
ticularly sensitive. 

SYMPTOMS. 

The  classical  pathognomonic  symptoms  of  exophthalmos  are  the 
well-known  triad  of  struma,  tachycardia,  and  exophthalmos, 
or  the  tetrad  of  struma,  tachycardia,  exophthalmos,  and 
tremor. 

These  are  well  described  by  Parry  (1815)  in  his  first  case,  a  married  woman,  aged  37, 
who  had  "  caught  cold  in  lying  in,  and  for  a  month  suffered  under  a  very  acute  rheumatic 
fever.  Subsequently  she  became  subject  to  more  or  less  palpitation  of  the  heart 
very  much  augmented  by  bodily  exercise,  and  gradually  increasing  in  force  and  frequency 
till  my  attendance,  when  it  was  so  violent  that  each  systole  shook  the  whole  thorax.  Her 
pulse  was  196  in  a  minute,  very  full  and  hard,  alike  in  both  wrists,  irregular 
as  to  strength,  and  intermitting  at  least  once  in  six  beats.  .  .  .  Twice  or  thrice  she  had 
been  seized  in  the  night  with  a  sense  of  constriction  and  difficulty  in  breathing, 
which  was  attended  with  spitting  of  a  small  quantity  of  blood.  She  described  herself  also 
as  having  frequent  and  violent  stitches  of  pain  about  the  lower  part  of  the 
sternum  .  .  .  .  About  three  months  after  lying  in,  while  she  was  suckling  her  child,  a 
lump   about  the  size  of  a  walnut  was  perceived  on  the  right  side  of  her  neck.     This 


THYROID    HEART.  581 

continued  to  enlarge  till  the  period  of  my  attendance,  when  it  occupied  both  sides  of  her 
neck  so  as  to  have  reached  an  uncommon  size,  projecting  forward  before  the  lowei  angle 
of  the  jaw.  The  part  swelled  was  the  thyroid  gland.  The  carotid  arteries  on 
both  sides  were  greatly  distended,  the  eyes  were  protruded  from 
their  sockets,  and  the  countenance  exhibited  an  expression  of  agitation 
and  distress,  especially  on  any  muscular  exertion,  which  I  have  rarely  seen  equalled.  .  .  . 
Bowels  were  usually  lax.  .  .  .  For  a  week  she  has  had  oedematous  swelling  of 
her  legs  and  thighs."    (The  patient  died  with  symptoms  of  heart  failure.) 

Besides  the  pathognomonic  triad,  increased  nervous  excitability, 
tremor,  loss  of  weight,  and  pigmentation  of  the  skin,  especially  about  the 
eyelids,  are  important  accessory  symptoms. 

The  chief  symptoms  of  Basedow's  disease  may  be  grouped  in  the  fol- 
lowing categories,  and  arranged  in  what  is  approximately  the  order  of 
increasing  severity. 

Cardiac  Phenomena.  —  Palpitation,  continuous  slight  elevation  of 
pulse-rate,  with  occasional  attacks  of  intense  tachycardia  brought 
on  by  emotion,  excitement,  or  exercise,  or  occasionally  on  awak- 
ening; visible  pulsation  and  dilatation  of  carotid  arteries;  pulse 
collapsing;  angina  pectoris;  hypertrophy  of  the  heart;  precordial 
heaving  and  intense  pulsation;  irregularity  of  pulse;  dilatation 
of  heart;  heart  failure;  ascending  oedema,  etc. 

Psychic  Symptoms.  —  General  nervousness,  insomnia,  restlessness, 
mental  exuberance  alternating  with  depression  and  melancholia, 
delusions  and  hallucinations. 

Ocular.  —  Staring  gaze  without  winking  for  considerable  periods. 
Widening  of  palpebral  slit  (Dalrymple,  v.  Stellweg's  sign),  lids 
do  not  follow  eyeballs  perfectly,  a  white  streak  of  sclera  is  seen 
between  lid  and  cornea,  especially  on  glancing  downward  or 
upward  (v.  Graefe's  sign),  inability  to  converge  in  looking  at 
near  objects  (Mobius'  sign),  exophthalmos,  overflow  of  tears, 
pain  and  feeling  of  tension  in  the  eyeballs,  corneal  ulceration. 

Peripheral  Nerve  Symptoms.  —  Fine  tremor  (from  8  to  10  per  second), 
especially  of  the  finger  tips,  nystagmus,  superficial  and  cog- 
wheel breathing,  astasia-abasia,  hyperesthesias  and  paresthesias 
occasionally,  inability  to  frown  or  wrinkle  forehead  (Joffroy's 
sign). 

Cutaneous  from  vasodilation  and  anti-adrenalin  action) .  —  Feeling 
of  heat,  continuous  and  intense;  lowered  electrical  resistance; 
sweating;  color  usually  pale  brownish — Addison-like  pigmenta- 
tion, especially  about  eyelids  (Jellinek) ;  flushes;  localized  transi- 
tory oedema,  especially  about  eyelids;  scleroderma. 

Nutritional  (increased  rapidity  of  metabolic  processes — loss  of  N  and 
PjOp). — Loss  in  weight;  sometimes  absolute  anorexia,  sometimes 
excellent  appetite;  attacks  of  diarrhoea,  often  with  slimy  stools; 
polyuria;  glycosuria.      Fever  (varying  from  99°  to  104°). 

Blood. — Slight  leucocytosis  without  change  in  red  blood-corpuscles 
or  secondary  anaemia;  polymorphonuclears  50-55  per  cent.,  lym- 
phocytes 20-25  per  cent.,  large  mononuclears  8-16  per 
cent,  (large  mononulcear  leucocytosis  present  in  formes  frustes). 
(Barker,  Caro.) 


582  DISEASES   OF  THE   HEART    AND    AORTA. 

Psychic  Manifestations. — The  psychic  symptoms  in  hyperthyroidism 
have  been  very  aptly  compared  to  the  well-known  effects  of  over-indul- 
gence in  coffee, — increased  activity  of  thought,  restlessness,  irritability, 
insomnia,  and  in  the  more  severe  cases  garrulity  and  delusions.  As  men- 
tioned above,  over-indulgence  in  coffee  may  sometimes  be  followed  by 
enlargement  of  the  thyroid.  There  can  be  little  doubt  that  many  cases  of 
so-called  neurasthenia  and  hysteria  are  due  to  a  more  or  less  transitory 
state  of  over-secretion  of  the  thyroid.  This  is  particularh'  true  when  the 
symptoms  are  accentuated  at  the  menstrual  periods,  for  then  the  thyroid 
secretion  is  increased.  It  is  possible  that,  as  suggested  by  Graves,  the 
"globus  hystericus"  may  be  due  to  an  acute  swelling  (erectile  expansion) 
of  the  thyroid.  Neurasthenic  symptoms  may,  however,  have  a  basis  in 
hyperthyroidism  in  cases  when  this  would  be  least  expected.  For  example, 
a  young  physician  in  robust  health  recently  complained  to  the  writer  of 
having  suffered  from  insomnia  and  palpitation  for  several  months,  during 
which  time  he  had  been  compelled  to  forego  his  accustomed  daily  exercise. 
On  closer  observation,  however,  he  observed  that  at  about  the  time  his 
symptoms  had  begun  he  noticed  a  slight  swelling  of  his  thyroid  which  had 
persisted  ever  since,  although  he  had  no  tremor. 

Cardiac  Signs  and  Symptoms.  —  The  cardiac  symptoms  also 
have  some  similarity  to  those  of  an  overdose  of  coffee,  especially  the  pal- 
pitation. This  symptom  is  probably  due  to  the  direct  stimulation  of  the 
afferent  nerves  of  the  heart  (depressor),  which  has  been  shown  by  v.  Cyon 
to  result  from  injection  of  thyroid  extracts,  iodothyroin  and  thyreoglobulin. 
Palpitation  is  the  earliest  and  often  the  mort  severe  symptom. 

The  tachycardia,  like  most  of  the  signs  of  Basedow's  disease, 
results  from  the  stimulation  of  the  accelerator  nerves  and  from  the  degree 
to  which  this  outweighs  the  effect  upon  the  vagus.  The  pulse-rate  may 
be  continuously  elevated  (over  120),  or  the  tachycardia  may  be  latent 
and  attacks  of  rapid  pulse  may  be  brought  out  only  by  slight  disturbance 
of  the  equilibrium  or  by  the  administration  of  very  minute  doses  of  thyroid 
extract  (Emerson,  quoted  by  Barker).  In  these  attacks  the  pulse- 
rate  rises  gradually  during  a  few  minutes  and  falls  gradually 
(in  contrast  to  idiopathic  paroxj'smal  tachycardia),  but  in  one  case  v. 
Hoesslin  has  seen  sudden  doubling  and  sudden  halving  of  the  rate.  Stru- 
bing  has  found  that  pressure  upon  the  vagus  slows  the  rapid  heart  of  Base- 
dow's disease,  showing  that  there  is  no  paralysis  of  that  nerve. 

Although,  as  Cleghorn  has  shown,  thyroid  extract  increases 
the  force  and  size  of  cardiac  contraction  (the  increased 
pulse-pressure  shows  increased  cardiac  output),  the  persistent  over-stimu- 
lation of  this  organ  draws  so  much  upon  its  reserve  force  that  it  may  readily 
suffer  from  overstrain  and  undergo  acute  dilatation.  Afferent  impulses 
through  the  depressor  nerves,  which  are  already  in  a  state  of  increased 
irritability,  may  give  rise  to  symptoms  of  typical  angina  pectoris,  with 
referred  pain  down  the  arms  and  precordial  hypersesthesia.  This  thyroid 
type  of  angina  pectoris  has  been  described  on  page  293.  Prolonged 
overstrain  may  result  in  failure  of  either  the  left  or  the  right  heart,  and 
symptoms  of  pulmonary  or  systemic  decompensation  (oedema,  ascites, 
etc.)  set  in. 


THYROID   HEART.  583 

The  irregularity  is  probably  due  to  occasional  extrasystoles, 
though  careful  analyses  of  its  nature  are  lacking.  In  one  case  reported  by 
V.  Hoesslin  there  was  definite  paroxysmal  tachycardia  with  sudden  onset 
and  sudden  cessation — approximate  halving  and  doubling  of  rate,  but 
Hirschfelder  finds  that  this  condition  is  a  rare  one  in  Basedow's  disease. 
The  attacks  of  tachycardia  and  palpitation  most  commonly  begin  and  end 
by  a  gradual,  though  rapid,  change  of  rate,  and  indicate  a  simple  exaggera- 
tion of  physiological  variations. 

The  maximal  blood-pressure  is  usually  high,  the  minimal 
normal;  the  pulse-pressure  increased;  this  shows  that  there  is  an  increased 
systolic  output  with  low  peripheral  resistance,  and  corresponds  well  with 
the  experimental  results  from  injection  of  thyroid  tissue  juice  (Pressaft). 
In  10  cases  of  Basedow's  disease  Krause  and  Friedenthal  found: 

Lowest.  Average.  Highest. 

Cm.  H2O.    Mm.  Hg.        Cm.  H2O.    Mm.  Hg.       Cm.  H2O.     Mm.  Hg. 

Maximal  blood-pressure ..  .     145  106  182  134  215  158 

Minimal  blood-pressure ...      85  62  89 . 5        65 . 8  90  66 

This  accords  with  the  writer's  experience,  but  in  the  early  cases  and 
"formes  frustes"  the  maximal  pressure  may  not  be  elevated  even  w^hen 
there  is  tachycardia. 

The  heart  is  usually  enlarged  and  hypertrophied,  the  apex  impulse 
forcible,  and  the  large  systolic  excursions  impart  a  heaving  to  the  whole 
chest.  In  periods  of  overstrain  from  exertion  or  excitement  there  may  be 
transitory  dilatation  of  the  heart,  and  this  uniformly  occurs  during  the 
chronic  heart  failure.  There  is  often  a  blowing  systolic  murmur  heard 
over  both  ventricles  and  at  the  apex,  perhaps  due  to  functional  insuffi- 
ciencies of  the  auriculoventricular  valves. 

Heart  failure  is  the  immediate  cause  of  death  in  most  cases  of  Base- 
dow's disease. 

Ocular  Manifestations. — The  ocular  manifestations  are  peculiar  and 
very  characteristic.  V.  Graefe  (1857)  called  attention  to  the  fact 
that  when  the  eyes  moved  upward  and  downward  the  lids 
did  not  follow  them  perfectly,  but  a  streak  of  white  sclera  could 
be  seen  between  lids  and  cornea  (Graefe's  sign).  Dalrymple  and  in 
1867  V.  Stellwag  noted  the  widening  of  the  palpebral 
slits,  the  staring  expression,  the  absence  of  winking.  V.  Stellwag's 
sign  is  in  most  cases  the  earliest  characteristic  sign  of  Basedow's  dissase. 
Mobius'  sign  is  the  inability  to  converge  the  two  eyes  when 
looking  at  a  very  near  object. 

The  origin  of  these  signs  is  very  simple.  Claude  Bernard,  when  he  first 
stimulated  the  cervical  sympathetic,  demonstrated  that  widen- 
ing of  the  palpebral  slit  and  dilatation  of  the  pupil  resulted 
and  that  the  eyeball  was  pushed  forward.  Aran  and  Kaufmann  (1860) 
demonstrated  that  this  exophthalmos  resulted  from  stimulation  of  Miiller's 
non-striated  muscle  in  the  eyelid,  which  is  innervated  by  the  cervical  sympathetic. 
These  experiments  were  confirmed  by  a  number  of  writers,  especially  MacCallum  and  Cor- 
nell (1904).  The  exact  course  of  the  fibres  of  Miiller's  muscle  and  their  mode  of  operation 
has  been  described  by  Landstrom.  Landstrom  finds  that  the  fibres  of  smooth  muscle 
form  a  narrow  cuff,  or  truncated  cone,  encircling  the  anterior  portion  of  the  orbit.  The 
fibres  at  the  posterior  border  of  the  cuff  pass  backward  and  are  inserted  into  the  sclerotic 
coat  of  the  eyeball.    The  fibres  forming  the  anterior  margin  of  the  cuff  are  inserted  into  the 


584 


DISEASES   OF   THE   HEART    AND    AORTA. 


upper  or  lower  lids,  in  which  they  run  obliquely  toward  the  palpebral  slit.  The  middle 
portion  of  the  cuff  constitutes  the  fixed  point  from  which  the  muscle  acts,  and  is  attached 
by  short  fibrous  bands  to  the  bony  wall  of  the  orbit.  Contraction  of  this  muscle 
therefore  tends  to  draw  the  eye  forward  (exophthalmos)  as  well 
as  to  pull  the  lids  apart  (Dalrymple  and  v.  Stell  wag's  sign). 
The  delicate  coordination  of  lid  movement  and  eye  movement 
is  disturbed  by  this  added  traction  upon  the  lid  (v.  Graefe's 
sign).  Moreover,  the  contraction  of  these  fibres  tends  to  keep 
the  axes  of  the  eyes  divergent,  and  thus  antagonizes  conver- 
gence   (Mobius'   sign). 


Fig.  324. — Diagram  showing  the  relation  of  the  various  anatomical  structure.s  concerned  in  the 
production  of  the  ocular  and  cardiac  manifestations  of  Basedow's  disea.«e.  A.  Distribution  of  the  branches 
of  the  cervical  s>Tnpathetic  to  the  heart,  thyroid  gland,  and  eyelids.  The  arrows  indicate  the  direction  in 
which  stimulation  of  the  cervical  sympathetic  moves  the  eyelids  and  eyeball.  SYMP  N,  sjinpathetic  nerve 
plexus;  SUP.  C.  GANG,  MID.  C.  GANG,  INF.  C.  GANG,  superior,  middle,  and  inferior  cen  ical  ganglia. 
B.  Relation  of  MuUer's  muscle  to  the  eyeball  and  structures  within  the  orbit  (schematic).  Miiller's  muscle 
(MVLL)  is  shown  in  black.  The  arrows  indicate  the  direction  of  its  pull.  TEND,  tendinous  attach- 
ment of  Muller's  muscle  to  the  orbit,  septum  orbitale  (SEPT.  ORB).  C.  Section  through  the  lateral 
portion  of  the  orbit  (semi-schematic,  modified  from  I^andstrom).  ORB,  orbitalis;  LEV,  levator  palpe- 
brarum;   CON  J,  conjtinctiva;   SCLER,  sclera;    RECT  MED,  rectus  medius. 


Muscular  Changes. — A  fine  tremor  beginning  in  the  fingers,  with  8-10 
contractions  per  second,  has  been  shown  by  Marie  to  be  almost  common 
enough  to  be  included  among  the  cardinal  symptoms.  It  is  probably  due 
to  the  overstimulation  of  the  peripheral  nerves,  and  finds  its  analogue  in 
the  tremor  from  coffee  and  tobacco.  Tremor  of  the  tongue  and  sudden 
movements  of  the  tongue  and  lips  are  not  as  common  as  in  alcoholism.  It 
is  probable  that  the  muscular  weakness  consequent  upon  the  katabolism 
of  muscle  proteid  aids  in  the  tremor. 

Astasia  abasia  (giving  way  of  the  legs  in  standing  and  walking)  is  rare, 
but  has  been  reported.   It  represents  an  extreme  grade  of  nervous  disturbance. 

The  increased  metabolism  of  X  and  P2O.,  with  destruction  of  muscle 
tissue,  fat,  and  to  a  lesser  extent  of  the  bones,  is  important  and  finds  its 
expression  in  the  general  loss  of  weight  (often  25  to  50  pounds).  It  is  the 
direct  result  of  iodothyrin  intoxication. 


THYROID    HEART.  585 

Diarrhoea  is  common.  There  is  often  a  good  deal  of  mucus  in  the  stools, 
suggesting  some  relation  to  the  so-called  mucous  colitis. 

Changes  in  the  Thyroid  itself. — As  regards  the  size  and  appearance  of 
the  thyroid  gland  there  is  great  variation.  In  spite  of  the  common  term 
of  "exophthalmic  goitre,"  the  thyroid  may  not  be  prominent  nor  even 
palpable.  Since  there  is  great  variation  in  the  average  size  and  weight  of 
the  thyroid  in  different  regions, — 25  to  33  Gm.  in  certain  regions,  60  Gm. 
in  others,  100  Gm.  in  Switzerland  (Oswald), — a  merely  palpable  thyroid 
need  be  of  no  diagnostic  importance.  Increase  in  the  size  of  the  thyroid 
is  equally  difficult  to  interpret.  The  size  of  the  thyroid  bears  a  definite 
relation  to  sexual  activity,  and  increases  regularly  during  menstruation 
and  pregnancy,  often  to  a  considerable  degree.  Indeed,  in  some  cases  of 
formes  frustes  it  is  not  unlikely  that  we  are  dealing  with  slight  hyperthy- 
roidism whose  intensity  is  determined  by  these  physiological  factors. 
Increased  vascularity  is  of  great  importance  in  differentiating  between 
transitory  and  persistent  hyperthyroidism.  It  can  be  demonstrated  by 
eliciting  a  murmur  and  thrill  over  the  thyroid  when  the  gland  is  pressed 
upon  (Guttmann).  This  cannot  be  produced  in  simple  goitres  or  normal 
glands. 

SECONDARY    HYPERTHYROIDISM. 

Moreover,  it  is  probable  that  in  many  neurotic,  toxic,  and  organic 
diseases  the  actions  of  nerves  or  of  hormones  arouse  the  thyroid  to  a  second- 
ary activity,  which  may,  nevertheless,  be  of  great  importance  in  determining 
the  features  of  the  case.  For  example,  Holz  has  reported  two  cases  of  exoph- 
thalmic goitre  in  children  in  whom  the  disease  subsided  on  removal  of  the 
adenoids;  one  case' recurred  and  again  subsided  with  the  recurrence 
and  removal  of  the  adenoids.  Accordingly  it  is  advisable  not  only  to  treat 
the  Basedow's  disease  but  also  to  look  for  and  treat  the  other  foci  of  excita- 
tion. 

DIAGNOSIS. 

It  is  evident  that,  though  there  can  be  little  doubt  as  to  the  nature 
of  well-developed  thyroidism,  there  may  be  room  for  much  debate  regarding 
cases  of  formes  frustes,  for  these  cases  must  be  differentiated  from  simple 
physiological  hypoactivity  of  the  thyroid.  Patients  should  be  carefully 
watched  for  the  development  of  ocular  signs,  especially  at  menstruation, 
since  these  are  practically  never  present  in  persons  whose  thyroid  activity 
is  normal. 

In  cases  in  which  symptoms  are  so  mild,  however,  it  is  still  important 
to  bear  in  mind  the  possibility  of  a  thyroid  origin  for  the  condition,  at 
least  in  so  far  as  an  increased  thyroid  secretion  may  arise 
reflexly  and  perpetuate  itself  through  the  vicious 
circle  mentioned  on  page  579.  It  is  probable  that  on  this  basis  the 
origin  of  many  an  obscure  "cardiac  neurosis"  will  be  cleared  up.  Hyper- 
thyroidism and  hysteria,  sexual  neurasthenias,  epilepsy,  tobacco  poisoning, 
alcoholism,  myocardial  disease,  and  valvular  diseases  are  frequently  asso- 
ciated, and  when  one  of  these  conditions  is  present  it  still  remains  important 
to  look  out  for  contributing   roles  on  the  part  of  the  thyroid. 


586  DISEASES   OF   THE   HEART    AND    AORTA. 

Each  case  of  morbus  Basedowii  may  be  considered  as  an  autointoxi- 
cation due  to  the  passage  of  more  or  less  iodized  thyreoglobulin  from  the 
thyroid  gland  into  the  blood.  When  this  is  secreted  in  large  quantities, 
the  condition  is  outspoken  and  presents  many  of  the  symptoms,  among 
them  some  of  severe  grade.  When  but  little  excess  of  thyreoglobulin 
circulates  in  the  blood,  it  may  give  rise  to  the  "  formes  frustes"  with  but 
few  symptoms  and  those  of  the  milder  type  predominating. 

However,  even  in  the  most  atypical  cases  of  "  forme  fruste  "one  or 
more  of  these  symptoms  may  reach  excessive  sever- 
ity, and  the  disease  may  persist  in  the  form  of  a  cardiac  neurosis,  a  psycho- 
sis, a  chronic  enteritis,  a  progressive  inanition,  a  diabetes,  or  even  a  mild 
relapsing  fever,  for  long  periods.  The  cardinal  suggestive  signs  may  be 
so  slight  in  intensity  as  to  be  noticed  only  when  the  suspicion  of  Basedow's 
disease  has  once  been  aroused  in  the  mind  of  the  examiner,  and  then  the 
coexistence  of  several  unobstrusive  features  may  make  the  condition  defi- 
nite; as,  for  example,  a  slight  staring,  anxious  expression  in  a  thin,  nervous 
woman  who  suffers  from  attacks  of  palpitation  and  precordial  pain  and 
who  manifests  a  slight  fine  tremor  of  the  fingers  and  a  tendency  to  diar- 
rhoea. On  closer  examination  it  may  be  found  that  the  lids  do  not  follow 
the  eyeballs  perfectly  and  there  is  slight  fulness  of  the  neck,  but  none  of 
these  symptoms  are  striking. 

Case  of  Basedow's  Disease  with  Anginal  Attacks. 

Mrs.  K.  M.,  housewife,  aged  23,  seen  under  treatment  at  the  Johns  Hopkins  Medical 
Dispensary  on  Dec.  29,  1906,  when  she  complained  of  palpitation  of  the  heart  and 
pain  in  the  right  chest  going  down  the  arm.  She  is  quite  nervous  and  sometimes  has 
crying  spells. 

She  is  a  rather  pale  woman,  fairly  nourished.  The  gums  and  mucous  membranes  are 
a  trifle  pale.  The  palpebral  slit  is  wider  than  normal,  but  lids  follow  eyes.  Convergence 
is,  however,  not  perfect.  The  outlines  of  the  thyroid  gland  can  be  seen;  the  gland  is  readily 
palpable,  but  not  much  enlarged.  The  lungs  were  clear  on  auscultation  and 
percussion. 

The  heart  was  not  enlarged;  sounds  clear.  Pulse  of  good  volume,  regular  in  force 
and  rhythm;  blood-pressure  apparently  low. 

She  was  given  Blaud's  pills  and  also  tincture  of  aconite  0.3  c.c.  (^v)  gind  potassium 
bromide,  without  relief.  She  was  seen  a  number  of  times  during  the  course  of  the  next 
year,  during  which  she  passed  through  a  normal  pregnancy  and  labor.  Palpitation 
continued.  A  well-marked  exophthalmos  developed  and  palpebral  slits 
became  a  little  wider  than  normal. 

During  April,  1907,  she  had  attacks  of  pain  over  the  left  side  of  the  chest 
and  down  the  front  (extensor  surface)  of  the  left  arm,  sometimes  radiating  to  the  shoulder. 
During  attacks  there  is  often  tenderness  in  the  fourth  left  interspace,  sometimes  also  in 
the  fifth,  about  the  mammillary  line.  It  never  radiates  to  the  right  of  the  midline.  These 
attacks  are  accompanied  by  palpitation  and  the  heart-rate  is  rapid.  She  also  has  a  peculiar 
fluttering  sensation,  and  occasionally  an  irregular  beat  Tracings  at  this  period  showed 
normal  venous  and  carotid  pulse.  She  was  given  small  doses  of  ergotin  without  relief.  A 
week  later  she  was  given  calcium  lactate  0.6  Gm.  (gr.  x)  after  meals,  after  which 
she  began  to  feel  better  at  once,  though  never  relieved  by  any  other  medicine.  The  remedy 
was,  however,  far  from  specific,  and  the  old  symptoms  returned  in  spite  of  the  calcium 
lactate.  During  the  course  of  the  next  six  months  various  remedies  were  given,  none  of 
them  with  marked  effect.  It  seemed  to  both  patient  and  physicians,  however,  that  she 
experienced  a  distinct  improvement  in  symptoms  whenever  calcium 
lactate  was  given  and  distinct  retrogression  when  other  drugs  were  substituted. 
Operation  was  advised  but  not  consented  to,  and  the  patient  was  lost  sight  of. 


THYROID    HEART.  587 


ACUTE    BASEDOW  S    DISEASE    SIMULATING    MALIGNANT    ENDOCARDITIS. 

One  group  of  cases  to  which  attention  should  be  especially  directed 
are  those  of  very  acute  Basedow's  disease  with  fever,  prostration,  tachy- 
cardia, profuse  sweats,  sometimes  chills  and  slight  jaundice — a  clinical 
picture  very  closely  simulating  acute  endocarditis  (W.  G.  Thompson). 
These  cases  are  rather  rare,  but  very  grave.  The  diagnosis  depends  upon 
the  cardinal  symptoms  aided  by  a  negative  blood  culture. 

PROGNOSIS  AND  TREATMENT. 

Statistics  regarding  the  mortality  of  Basedow's  disease  vary  considera- 
bly, as  shown  by  the  following  list. 

V.  Dusch 12 . 5  per  cent. 

V.  Graefe    12      per  cent. 

Mackenzie  12 . 5-25  per  cent. 

Cheadle 9.6  per  cent. 

Billingham 18 . 1  per  cent. 

Gaill 21 .3  per  cent. 

Charcot 25      per  cent. 

Buschan  (900  cases) 12.5  per  cent. 

Thompson 10      per  cent. 

Williamson 25      per  cent. 

These  figures  err,  on  the  one  hand,  because  only  the  serious  cases  reach 
the  literature,  and,  on  the  other,  because  most  of  the  cases  have  been  fol- 
lowed for  only  short  periods.  Williamson,  who  followed  his  cases  for  some 
years  and  found  a  25  per  cent  mortality,  probably  approximates  the  truth. 
J.  Berry  gives  the  following  statistics  of  56  cases  treated  without 
operation : 

Complete  recovery 10 

Considerable  improvement 24 

Little  or  no  change 8 

Fatal 14 

Even  after  recovery  recurrence  is  the  rule,  so  that  as  ex- 
cellent an  observer  as  August  Hoffmann  states  that  in  23  outspoken  cases 
he  has  not  seen  a  single  permanent  recovery ! 

It  is  evident,  therefore,  that  at  the  onset  of  undoubted  Graves's 
disease  therapeutic  interference  is  necessary.  The  best  principles  in  inau- 
gurating treatment  are  those  which  may  be  deduced  from  the  findings  of 
V.  Cyon's  experiments, — i.e.,  that  the  clinical  manifestations  are  due  to 
hypersecretion  of  thyreoglobulin,  that  this  is  proportional  to  the  blood  flow 
through  the  thyroid,  and  that  the  thyroid  secretion  in  the  blood  tends 
itself  to  increase  this  flow  and  to  produce  a  vicious  circle. 

The  first  essential  of  any  palliative  treatment,  therefore,  is  to  reduce 
the  thyroid  secretion  to  its  lower  ebb  by  the  removal  of  the  two  stimulating 
causes — exercise  and  excitement.  In  the  mild  cases  a  simple  isolation  cure, 
with  absolute  rest  in  the  horizontal  position,  can  sometimes  so  lessen 
the  flow  through  the  thyroid  and  the  secretion  of  this  gland  by  diminishing 
the  size  and  number  of  heart-beats  that  the  thyreoglobulin  content  of  the 
blood  falls  to  normal  and  symptoms  subside.    If  the  rest  cure  be  prolonged, 


588  DISEASES   OF   THE   HEART    AND    AORTA. 

the  slight  glandular  hyperplasia  of  early  cases  may  subside  and  a  permanent 
cure  may  result. 

Various  measures  assist  this  process,  especially  those  which  act  as 
psychic  sedatives.  Psychotherapy  and  suggestion,  in  so  far  as 
they  tend  to  lessen  the  elements  of  worry,  quiet  the  patient's  mind,  and 
thus  quiet  his  heart's  action,  may  aid  in  tiding  over  a  period  of  not  too 
intense  excitement.  Similarly  Mobius,  the  apostle  of  serum  therapy, 
reports  the  cure  of  one  case  by  hypnotism !  These  are,  however,  exceptional. 
Psychotherapy  in  Basedow's  disease  is  to  be  classed  among  the  valuable 
sedative  measures,  but  not  among  those  of  fundamental  therapeutics. 
Cold  wet  packs,  especially  before  retiring,  may  be  of  considerable 
assistance  (Eichhorst),  as  also  the  bromides  and  the  soporifics  (veronal, 
trional,  etc.),  though  to  a  less  degree.  Calcium  salts  are  often  very 
satisfactory  as  sedatives.  The  iodobromide  of  calcium  was  used  by  Guptill 
(1874).  In  one  case  (K.  M.)  under  the  writer's  care  calcium  lactate  was 
the  only  drug  which  caused  any  symptomatic  relief,  but  even  this  was 
not  marked.  Miiller  and  others  have  used  quinine,  especially  as  the 
hydrobromate,  but  in  many  cases  it  is  without  effect. 

Iodine  as  used  by  the  earlier  observers  may  sometimes  exert 
a  positively  harmful  influence  by  activating  (iodizing)  still 
more  of  the  thyreoglobulin,  and  it  may  thus  bring  on  an  exacerbation  of 
the  condition.  The  effect  of  potassium  iodide  is  less  certainly  harmful 
and  is  sometimes  beneficial,  but  its  action  is  uncertain. 

Galvanization.  —  One  of  the  oldest  and  best  forms  of  treatment  is 
galvanization  of  the  cervical  sympathetic,  with  the 
anode  over  the  carotid  artery  and  the  cathode  at  the  nape  of  the  neck. 
With  currents  of  2-3  milliamperes,  as  used  by  Chvostek,  Benedikt,  Car- 
dew,  and  others,  it  uniformly  gives  a  certain  degree  of  improvement, 
without  effecting  a  cure.  In  early  cases  J.  O.  Hirschfelder  has  obtained 
complete  subsidence  of  symptoms  in  a  considerable  number  of  patients  by 
the  use  of  strong  currents  (20-30  milliamperes),  the  negative  pole  being 
applied  over  the  sympathetic  at  the  neck,  the  positive  over  the  thyroid  for 
two  or  three  minutes.  After  this  it  is  applied  over  the  heart.  This  vigorous 
treatment  seems  to  be  the  best  method  of  applying  electricity,  but  must 
be  continued  for  several  months. 

X=Rays.  —  Exposure  of  the  thyroid  to  the  Ron  t  gen 
rays  was  introduced  by  Pusey,  Boggs,  and  Beck  in  America,  and  has  had 
in  the  main  a  favorable  action.  Schwarz  (1908)  collected  reports  of  40 
cases,  showing  gain  in  26,  improvement  in  nervous  symptoms  in  40, 
exophthalmos  better  in  15,  but  struma  lessened  in  only  8. 

Specific  Sera. — Two  forms  of  so-called  specific  sera  are  also  in  use: 
(1)  anti-thyreoidin  (thyroidectin),  the  serum  of  thyroidectomized  sheep 
(Mobius),  has  been  in  use  for  some  years,  and  in  spite  of  numerous  favorable 
reports  has  been  found  absolutely  without  effect  by  Ewald,  Mackenzie, 
and  Striimpell.  (2)  Beebe  has  prepared  an  antiserum  for  the  nucleo- 
proteid  of  the  thyroid  gland  from  animals  into  which  the  purified  nucleo- 
proteid  thyreoglobulin  had  been  injected,  in  the  hope  of  bringing  about 
retrogressive  changes  in  this  gland.  This  serum  has  been  used  therapeu- 
tically by  Rogers  and  by  W.  G.  Thompson,  who  report  distinctly  favorable 


THYROID    HEART.  589 

results,  especially  in  the  very  acute  cases  (90  cases:  23  cured,  54  improved, 
1 1  failed,  4  died) ;  but  other  observers  state  that  the  results  are  no  better 
than  those  in  ordinary  hospital  practice,  and  further  confirmation  is  needed. 
Operative  Treatment. — Thyroidectomy. — The  physiological  indication 
for  therapy  in  Basedow's  disease  is  to  lessen  the  amount  of  thyreoglob- 
ulin secreted  into  the  blood.  If  the  various  methods  intended  to  affect 
the  gland  as  a  whole  are  unsuccessful,  the  secretion  may  be  diminished  by 
removing  a  large  portion  of  the  gland  (thyroidectomy).  This  operation 
was  first  successful  in  the  hands  of  L.  Rehn  (1884),  and  has  now  come 
into  quite  general  use,  especially  through  the  work  of  Mickulicz  and  the 
Kochers  in  Europe,  and  Halsted  and  the  Mayos  in  America. 

The  operation  should  be  done  under  local  cocaine  anaesthesia.  It  may  vary  from 
ligature  of  the  arteries  to  one-half  of  the  gland,  or  this  may  be  combined  with  excision  of 
the  latter;  or,  on  the  other  hand,  one-half  of  the  gland  may  be  excised  and  the  arteries 
supplying  a  portion  of  the  other  may  be  ligated.  The  technic  and  results  in  large  series 
of  cases  have  been  reported  by  A.  Kocher,  Landstrom,  and  C.  H.  Mayo,  and  many  of  the 
important  details  by  Halsted  and  Evans. 

Kocher  (1907)  especially  calls  attention  to  the  necessity  of  suiting 
the  extent  of  the  operation  to  the  condition  of  the  patient,  especially  the 
cardiovascular  condition.  "A  systolic  blood-pressure,  even  of  195  mm. 
Hg,  does  not  forbid  operation;  .  .  .  but  if  we  find  the  blood-pressure 
below  normal  and  the  disease  highly  developed,  we  must  study  the  condi- 
tion and  especially  note  the  action  of  the  heart  after  exercise  or  excite- 
ment. Under  these  circumstances  we  might  find  a  sudden,  very  marked 
dilatation  of  the  heart,  irregularity  of  pulse,  and  a  blood-pressure  which 
cannot  be  measured  by  our  ordinary  methods." 

The  patient  should  be  given  a  preparatory  period  of  rest  and  pallia- 
tive treatment  to  prepare  her  for  the  operation,  and  two  or  more  opera- 
tions should  be  done  on  the  same  patient  rather  than  too  extensive  an  opera- 
tion at  one  sitting.  Kocher  never  ligates  more  than  two  arteries  nor  re- 
moves more  than  one-half  the  gland  at  one  sitting,  but  these  measures 
suffice  in  cases  that  are  not  too  far  advanced.  Halsted  has  called  particular 
attention  to  the  need  of  preserving  the  parathyroid  gland 
in  order  to  avoid  tetany.  Hence  he  advocates  tracing  out  the 
branches  to  these  small  bodies  and  then  ligating  the  main  artery  beyond 
them.  Both  Kocher  and  Halsted  insist  upon  the  greatest  care  in 
the  ligation  of  all  bleeding  points  during  the  opera- 
tion and  in  draining  off  any  small  collection  of  ser um 
which  may  collect  during  the  healing  of  the  wound.  This  greatly  diminishes 
or  obviates  the  intensification  of  Basedow  symptoms  which  sometimes 
result  a  few  days  after  operation  (probably  from  absorption  of  iodothyreo- 
globulin  upon  the  raw  surface  of  the  gland)  and  which  may  be  dangerous. 
Halsted  also  found  that  the  continuous  use  of  an  ice-bag  upon  the  neck 
during  a  few  days  after  the  operation  retards  the  absorption  from  the  gland 
and  lessens  the  frequency  of  these  symptoms. 

As  a  result  of  this  procedure  in  254  patients  (2  operations  in  71  cases), 
A.  Kocher  has  obtained  great  improvement  in  every  case,  with  abso- 
lute and  permanent  cure  in  8  3  per  cent.,  and  3.5  per 
cent,  of  deaths.     In  the  last  91  operations,  since  the  above  precautions 


590  DISEASES   OF   THE    HEART    AND    AORTA. 

had  been  observed,  he  has  not  had  a  single  death!  C.  H.  Mayo  had  9 
deaths  in  176  cases,  but  only  one  in  his  last  75;  and  Professor  Halsted's 
results  at  Johns  Hopkins  are  equally  favorable. 

In  cases  of  long  standing  the  exophthalmos  never  disappears,  for  the 
depths  of  the  orbit  have  become  filled  with  fat  which  continues  to  push 
the  eye  forward  after  the  contraction  of  Miiller's  muscle  has  subsided. 

Hypertrophy  of  the  heart  and  secondary  myocardial  changes  also 
remain,  perhaps  some  cardiac  weakness,  but  these  are  greatly  diminished 
when  the  continuous  cardiac  excitation  is  removed. 

It  must  be  admitted  also  that,  as  Tinker  states,  the  operation  requires 
more  skill  and  practice  than  most  surgical  procedures,  and  the  prognosis 
is  therefore  far  better  done  by  a  man  whose  experience  in  this  line  is  con- 
siderable than  by  a  surgeon  of  even  excellent  local  reputation. 

As  regards  the  indication  for  operation,  Kocher  believes  that  ''dis- 
tinct vascular  symptoms  (other  than  mere  palpita- 
tion and  tachycardia)  should  at  once  induce  surgical 
treatment.''  Before  these  have  set  in,  the  palliative  method  may  be 
used  for  a  while,  and  many  cases  may  be  relieved  thereby  or  subject  only 
to  occasional  recurrences.  Should  the  mental  symptoms  and  tachycardia 
persist  or  become  more  severe,  the  physician  should  recommend  operation 
while  the  patient's  general  condition  is  still  good,  and  should  not  wait 
until  she  is  a  complete  physical  wreck  before  turning  over  the  responsibility 
to  the  surgeon.  The  surgeon  should  be  allowed  to  operate  upon  the  early 
but  chronic  cases  which  do  not  improve  under  palliative  treatment. 

These  rules  apply  as  well  to  the  cases  of  "formes  frustes"  as  to  the 
outspoken  Basedow's  disease.  The  persistence  of  psycho-  and  cardio- 
neuroses  gives  the  indications,  v/hether  all  the  cardinal  features  are  pro- 
nounced or  not,  and  spontaneous  recovery  is  no  more  likely  to  occur  after 
the  "  forme  fruste "  has  persisted  than  in  cases  where  all  the  signs  are  well 
marked. 

Sympathectomy  ( Jonnesco's  Operation) .  —  Another  operation,  which 
has  been  performed  by  Jonnesco,  is  the  removal  of  the  sympathetic  ganglia 
on  both  sides  of  the  neck.  The  result  of  this  is  usually  an  immediate  slow- 
ing of  the  pulse,  and  often  a  cessation  of  other  symptoms.  Jonnesco  reports 
several  cases  of  permanent  cure,  but  in  the  hands  of  a  considerable  number 
of  later  observers,  among  them  Kocher,  good  results  have  been  lacking  or 
transitory,  and  this  method  should  therefore  be  cast  aside. 

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III. 

MISCELLANEOUS    DISTURBANCES    OF    CARDIAC    FUNCTION— 

THE    SO-CALLED    "CARDIAC    NEUROSES" 

AND    ''CARDIAC    NEURASTHENIA." 

GENERAL     CHARACTERISTICS. 

One  of  the  largest  groups  of  cases  seen  by  the  clinician  is  made  up 
chiefly  of  pale,  anaemic-looking  young  patients,  with  hollow  lustreless  eyes 
and  sunken  cheeks,  who  complain  of  symptoms  which  may  be  divided  into 
two  categories: 

Symptoms.  —  1.  Symptoms  referable  to  sensory  disturbances 
about  the  heart: — palpitation,  precordial  tenderness,  pain  or  constriction, 
pains  and  sensory  disturbances  down  the  arms,  and,  in  rarer  cases,  of 
attacks  resembling  angina  pectoris. 

2.  Symptoms  referable  to  motor  disturbances  of  the  circulation, 
and  especially  to  the  distribution  of  blood  in  the  body: — cardiac  arrhyth- 
mia, weakness,  lassitude  and  weariness,  vertigo,  muscse  volitantes,  fainting 
spells,  and  an  infinite  variety  of  psychasthenic  and  nervous  symptoms. 

This  same  symptom  complex  has  already  been  encountered  in  the 
attacks  of  paroxysmal  tachycardia  (Chapter  II.),  where  it  has  been  seen 
to  result  from  "arterial  ansemia,"  or  the  relative  depletion  of  the  arteries 
through  dilatation  of  the  veins,  especially  in  the  splanchnic  region.  Y. 
Henderson  believes  that  under  these  conditions  the  viens  are  not  overfilled, 
but  that  they  too  have  become  depleted  by  transudation  of  fluid  into  the 
lymph  and  tissue  spaces.  Mr.  C.  C.  Cody,  in  the  Johns  Hopkins  medical 
clinic,  has  found  a  very  low  venous  pressure  (  —  2  to  —7  cm.  HjO)  in  a 
number  of  cases  of  neurasthenia  and  post-operative  asthenia  in  which  the 
above-mentioned  symptoms  were  present.  The  arterial  pressure  in  all 
but  one  of  these  cases  was  about  normal,  ranging  from  104  to  125  mm.  Hg. 
This  same  circulatory  state  seems  to  be  present  throughout  the  groups 
of  cases  about  to  be  discussed,  although  the  mechanisms  by  which  it  is 
brought  about  are  various. 

Changes  in  Rhythm. — Alterations  of  rhythm  are  very  common  in  this 
group  of  cases  (Hoffmann,  Mackenzie,  Reissner).  They  are  usually  associ- 
ated with  respiration,  with  a  slowing  of  the  pulse  during  inspiration  and  a 
quickening  during  expiration  (Fig.  325) .  It  will  be  noted  that  this  exactly 
corresponds  to  the  normal  centripetal  action  currents  in  the  vagus  (Eint- 
hoven,  Flohil  and  Battaerd)  which  occur  with  each  inspiration,  and  it  is 
probable  that  in  the  condition  of  heightened  excitability  this  (usually  sub- 
normal) reflex  stimulation  becomes  active.  Stadler  and  Hirsch  have  been 
able  to  produce  such  irregularities  by  inflating  the  intestines  of  dogs  and 
rabbits,  but  find  them  only  accompanying  dyspnoea.  These  observers  also 
found  that  such  inflations  of  the  intestines  were  always  accompanied  by  rise 
38  593 


594  DISEASES   OF   THE    HEART   AND    AORTA. 

of  blood-pressure.  The  writer  has  been  able  to  confirm  these  observations. 
Moreover,  McCaskey  and  Russell  find  that  an  elevation  of  30  or  40  mm. 
Hg  in  blood-pressure  may  occur  in  the  course  of  gastro-intestinal  troubles, 
especially  hyperchlorhydria  and  flatulence.  Russell  suggests  that  there  is 
a  relationship  between  chronic  gastric  intestinal  disturbances  and  sclerosis 
of  mesenteric  vessels. 

In  the  cases  of  enteroptosis  and  of  bathycardia  a  true  pulsus  para- 
doxus (diminution  or  dropping  of  beats  during  inspiration)  may  occur 
from  the  tugging  upon  the  mediastinum,  aorta,  and  great  veins  when  the 
diaphragm  is  drawn  down  during  inspiration.  In  rarer  cases,  and  espe- 
cially those  of  gastro-intestinal  origin,  small,  early  beats  resembling 
extrasystoles  are  present.  In  making  the  diagnosis  of  extrasy stoles, 
however,  great  care  must  be  used,  for  it  must  be  remembered  that  in  the 


1 
RESP. 

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RADIAL 

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1     Exp. 

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1     Exp.      1 

Insp. 

JOJs^ 

J-h^ 

Fi«.  325. — Respiratory  arrhythmia  in  a  young  cigarette  smoker. 

usual  rhythmic  variations  in  rhythm  the  last  beat  of  a  series  with  increasing 
rapidity  may  be  followed  by  the  pause  due  to  maximal  slowing,  and  thus 
an  extrasystole  may  be  simulated.  On  the  other  hand,  it  must  be  remem- 
bered that  no  experimenters  have  as  yet  been  able  to  produce  extra- 
systoles  by  stimulating  the  extrinsic  cardiac  nerves  (Hering,  Hoffmann,  the 
writer  and  others),  and  therefore  each  case  of  the  sort  should  be  carefully 
studied  with  venous  tracings  and  electrocardiograms.  True  ventricular 
extrasystoles  demonstrable  with  the  electrocardiogram  are  often  brought 
on  by  flatulence,  though  many  writers  agree  with  Friedrich  Miiller  that 
the  presence  of  definite  extrasystoles  is  indicative  of  myocardial  disease. 

Some  years  ago  the  writer  had  under  observation  a  man  forty  years  of  age  who  was 
subject  to  palpitation  and  an  arrhythmia  brought  on  whenever  he  developed  gas  in 
the  stomach  or  intestines.  He  himself  was  able  to  distinguish  " large  and  small"  beats 
among  the  palpitations,  and  tracings  with  modified  Erlanger  apparatus  from  veins  and 
arteries  bore  out  his  impressions.  It  is,  however,  difficult  to  decide  whether  these  small 
beats  represent  auricular  extrasystoles  or  whether  there  is  simply  a  rapid  rhythm  inter- 
rupted by  long  pauses  of  vagal  origin.  He  stated  that  nevertheless  he  was  able  to  "out- 
walk his  doctors"  at  hill  climbing  during  periods  when  he  was  suffering  from  both  palpita- 
tion and  arrhythmia.  A  moderate  dose  (i  mg.  =  gr.  ^^5)  of  atropine  caused  dryness  of  the 
mouth  and  some  vertigo,  but  did  not  greatly  alter  the  pulse-rate  nor  cause  the  arrhythmia 
to  disappear.  The  patient  would  not  allow  a  larger  dose  to  be  given.  If  one  could  be  certain 
that  this  dose  had  paralyzed  the  vagus  the  extrasystolic  nature  of  the  arrhythmia  would 
be  established,  but  it  is  most  probable  that  the  vagus  was  but  little  affected  and  that  this 
evidence  cannot  be  regarded  as  conclusive. 

It  has  long  been  customary  to  designate  such  cases  as  "cardiac 
neuroses,  or,  from  the  neurasthenic  symptoms  which  are  most  striking 
to  the  physician,  as  "cardiac  neurasthenia."  On  closer  exami- 
nation, however,  it  may  usually  be  found  that  both  the  cardiac 
and  the  neurasthenic    symptoms   are  not   primary,   but 


DISTURBANCES   OF   CARDIAC   FUNCTION.  595 

are  secondary  to  some  visceral  displacement  or  irri- 
tation, to  some  intoxication,  or  in  rarer  cases  to  some 
primary  intense  emotional  disturbance.  The  heart  itself 
is  sound,  but,  owing  to  the  distribution  of  blood,  does  not  get  a  chance 
to  do  the  work  of  which  it  would  be  capable.  The  terms  "  cardiac  "  and 
''neurasthenia"  are  therefore  both  misleading,  and  it  might  perhaps  be 
more  satisfactory  to  designate  such  conditions  by  the  adjective  "pseu- 
docardiac''  (" pseudocardiac  enteroptosis,"  " pseudocardiac  gastral- 
gia,"  "pseudocardiac  aerophagia,"  etc.). 

CLINICAL    GROUPINGS. 

Most  if  not  all  of  these  "  cardiac  neurasthenias  "  are  brought  on  by  the 
following  conditions: 

Alterations  of  the  position  of  the  heart  in  the  thorax. 

a.  Kyphoscoliosis,    narrowness  or  flatness  of  chest. 

b.  Cardioptosis   or  bathycardia  (low  heart), 

(1)  due  to  enteroptosis  (low  diaphragm), 

(2)  due  to  long  thorax  with  diaphragm  normal. 

c.  High   diaphragm   from 

(1)  flatus, 

(2)  fat, 

(3)  tight  lacing. 

Although  many  cases  arise  in  which  no  site  of  origin  can  be  found  for 
the  symptoms,  the  following  represent  a  few  of  the  more  common  causes: 

1.  Abnormal    position    of   the    heart, 

a.  From  curvature  of  the  spine. 

b.  From  pleural  adhesions. 

c.  Owing  to  a  low  diaphragm. 

2.  Visceral    reflexes. 

a.  Gastric,  oesophageal  and  intestinal. 

(1)  Air  swallowing. 

(2)  Gastritis,  gastralgias. 

b.  Sexual  organs. 

(1)  Sexual  excesses  (male  or  female). 

Female — At  onset  of  menses  and  at  menopause;  at  menstruation; 

from  myoma  and  other  lesions  of  generative  organs. 
Males — Gonorrhoea,  prostatitis,  masturbation. 

3.  Intoxications. 

Tobacco. 
Alcohol. 
Coffee.  _ 

4.  Anaemia.  ^ 

5.  Intense   emotional    disturbances. 


ALTERATIONS   IN   POSITION   OF   THE   HEART. 

DISPLACEMENT   OF   THE   HEART   FROM   MALFORMATIONS. 

The  displacement  of  the  heart  which  occurs  in  kyphosis  and  scoliosis 
is  often  the  cause  of  a  true  cardiac  weakness,  i.e.,  weakness  and  dyspnoea 
on  exertion  as  well  as  from  nervous  causes — a  so-called  constitutional  heart 
weakness  as  Kraus  terms  it. 


596 


DISEASES   OF   THE    HEART   AND    AORTA. 


The  patients  are  usually  pale,  rather  weak,  and  readily  become  ex- 
hausted and  cyanotic,  and  manifest  all  the  cardioneurotic  symptoms. 
The  actual  cause  of  the  trouble  lies  not  so  much  in  the  heart  as  in  the  posi- 
tion in  which  it  is  placed  in  the  thorax.     Pressure  and  tractions  upon  both 

the  vensB  cavse  and  the  arteries  render 
both  inflow  and  outflow  difficult,  and 
thus  bring  about  a  high  venous  and 
a  low  arterial  pressure,  with  the 
symptoms  which  follow  in  its  wake. 
Kraus  and  recently  Herz  have 
called  attention  to  the  cardioneurotic 
symptoms  which  occur  in  all  narrow- 
chested  individuals.  Herz  calls  atten- 
tion to  the  fact  that  in  such  cases 
there  is  a  tremendous  lifting  of  the 
ribs  and  precordium  with  each  sys- 
tolic erection  of  the  heart.  This  is 
due  to  the  short  anteroposterior  and 
especially  oblique  diameter  of  the 
chest,  so  that  the  heart  pivoted 
against  the  posterior  chest  wall  must 
push  out  the  left  anterior  wall  in  order  to  complete  its  systole  (cf.  Fig.  326). 
As  will  be  noted,  this  condition  is  quite  different  from  that  which  results 
from  the  low  diaphragm  or  from  cardioptosis,  for  in  those  conditions  the 
heart  either  beats  in  the  long  axis  of  the  thorax,  or  from  its  mobility  can 
adapt  itself  to  a  narrower  chest. 


Fig.  326. —  Cross  section  of  the  thorax  of 
a  flat-chested  individual,  showing  the  systolic 
heaving  of  the  chest  wall  (broken  lines)  and 
the  forces  bringing  it  about.  The  outlines  of 
the  chest  wall  and  heart  during  the  systolic 
heaving  are  shown  by  the  dotted  lines  and 
obliquely  shaded  areas.  The  protrusions  and 
retractions  are  shown  by  the  arrows. 


LOW  HEART. 

Even  when  there  are  no  malformations  of  the  chest,  conditions  arise 
in  which  the  position  of  the  heart  within  the  thoracic  cavity  is  altered, 
and  these  give  rise  to  cardioneurotic  symptoms.     These   conditions  are: 

I.  Cardioptosis  (wandering  or  movable  heart),  in  which  the  mediastinal 
attachments  are  loose  and  the  heart  readily  moves  from  side  to  side,  as 
well  as  up  and  down. 

II.  Bathycardia  (low  or  unsupported  heart),  in  which  the  heart  lies 
low  in  the  thorax  because  the  dome  of  the  diaphragm  is  lower  than  normal. 
This  is  sometimes  due  to  hepatoptosis  and  sometimes  to  a  congenitally 
low  liver. 

III.  The  high  heart  (high  diaphragm),  from  various  causes,  especially 
flatulence,  fat,  lacing,  and  during  pregnancy. 


MOVABLE    HEART    (CARDIO PTOSIS)  . 

Cardioptosis,  or  extreme  mobility  of  the  heart  as  shown  on  change 
of  position,  was  first  described  by  Glenard  (1885)  and  by  Cherchevsky 
(1887).  The  latter  observer  noted  that,  while  the  borders  of  the  normal 
heart  move  1-3  cm.  when  the  patient  turns  from  the  left  side  to  the  right 
(while  lying  down),  a  certain  number  of  cases  (2.4  per  cent,  of  all  cases, 
according  to  Einhorn)  are  encountered  in  which  it  moves  from  4-7  cm. 


DISTURBANCES   OF   CARDIAC   FUNCTION.  597 

without  any  other  changes  or  any  enlargement  of  the  heart.  As  a  rule, 
the  symptoms  date  from  some  time  when  the  patient  has  lost  in  weight, 
perhaps  because  the  disappearance  of  mediastinal  and  omental  fat  causes 
the  organs  to  become  looser  than  before.  Einhorn  has  found  it  much  more 
common  in  men  (18  cases)  than  in  women  (4  cases)  and  always  associated 
with  hepatoptosis;  though  in  cases  like  that  given  below  the  element  of 
hepatoptosis  may  be  absent. 

Case  of  Cardioptosis. 

This,  as  well  as  the  other  symptoms,  is  beautifully  illustrated  by  a  case  which  the 
writer  has  recently  seen  in  consultation  with  Dr.  L.  P.  Hamburger.  The  patient,  aged  31, 
had  been  a  trained  nurse  since  18.  Her  father  had  died  of  enlarged  heart  and  her  mother 
died  suddenly.  Except  for  scarlet  fever,  whooping-cough,  and  measles  as  a  child,  she  had 
been  perfectly  healthy  until  the  age  of  19,  when  a  dermoid  cyst  of  the  left  ovary  caused 
profuse  menstrual  bleedings.  This  was  removed  and  the  wound  drained.  Adhesions 
formed,  causing  headaches  and  backaches  and  finally  a  nervous  break-down,  so  that  a 
second  operation  was  done  nine  years  later  to  relieve  the  adhesions.  At  the  time  of  this 
operation  she  lost  14  pounds  and  was  very  nervous,  and  during  her  early 
convalescence  had  a  syncopal  attack  during  which  her  hands  and  forearms  became 
completely  blanched.  One  year  later  the  patient  felt  her  first  cardiac  symp- 
toms, suffering  palpitation,  and  when  lying  down  has  a  feeling  "as  though  the  heart 
were  turning  over  "  or  "  like  a  rubber  bulb  or  sponge  being  squeezed  out."  She  then  feels 
sick  and  has  a  feeling  of  oppression  in  the  chest. 

Physical  examination  shows  a  fairly  nourished  young  woman  of  good 
color;  pupils  equal  and  no  signs  of  Basedow's  disease.  The  left  lobe  of  the  thyroid  is  slightly 
hard,  but  that  organ  is  rather  small. 

The  thorax  is  quite  well  formed,  not  especially  flat.  Costal  angle  normal.  Lungs 
clear.  The  heart  is  not  enlarged  and  the  sounds  are  clear.  On  turning  from  side 
to  side,  however,  the  heart  moves  8  cm.  The  pulse  is  of  good  volume 
and  shows  a  well-marked  respiratory  irregularity  of  the  type  described  above,  but  no 
extrasystoles.  The  abdominal  walls  are  soft  but  not  especially  lax;  the  liver  does  not 
descend  when  the  patient  stands,  but  the  right  kidney  is  palpable. 

Bromides,  nitroglycerin,  and  strophanthus  have  been  without  avail;  tincture 
of  belladonna  has  somewhat  quieted  her  cardiac  symptoms.  The 
intensity  of  the  symptoms  seems  to  vary  with  her  general  condition.  Upon  being 
assured  of  the  trivial  nature  of  her  complaint,  her  symptoms 
immediately   disappeared. 

Several  months  later  she  reported,  however,  that  they  reappeared  from  time  to  time 
during  periods  when  she  was  fatigued  or  nervous.  The  presence  or  absence  of  symptoms 
was  always  quite  independent  of  the  mobihty  of  the  heart.  In  spite  of  her  gain  in  weight 
and  the  improved  condition  under  treatment,  the  cardiac  borders  moved  at  least  7  cm. 
during  the  periods  when  she  was  free  from  symptoms. 

Treatment.  —  The  treatment  of  cardioptosis  presents  a  number  of  dif- 
ficulties. As  seen  from  the  case  cited  above,  the  symptoms  depend  not 
only  upon  the  actual  mobility  of  the  heart  but  also  upon  the  general 
condition  of  the  patient's  nervous  system.  It  is  the  latter  which  deter- 
mines whether  or  not  the  afferent  impulses  from  the  heart  shall  reach  the 
threshold  of  consciousness.  Accordingly,  the  unpleasant  cardiac  sensa- 
tions may  be  present  only  when  the  irritability  of  the  nervous  system  is 
increased  by  ifatigue,  anaemia,  or  other  affections;  so  that  relief  of  the 
latter  by  general  measures  relieves  the  cardiac  symptoms  as  well,  without 
affecting  their  underlying  cause.  The  mobility  of  the  heart  itself  cannot 
be  treated  directly;  but  it  is  sometimes  possible,  by  overfeeding,  to 
cause  a  sufficient  deposit  of   fat  in   the    mediastinum    and    pericardium 


598 


DISEASES   OF   THE    HEART    AND    AORTA. 


to  diminish  the  movements  a  little.  Even  when  unsuccessful  in  this 
way,  however,  overfeeding  often  aids  by  improving  the  general  condition 
and  nervous  tone. 

GENERAL    SPLANCHNOPTOSIS. 

The  mechanism  which  gives  rise  to  the  cardiac  symptoms  of  splanch- 
noptosis (enteroptosis)  has  been  investigated  anatomically  by  Keith  and 
chnically  by  Wenckebach.  The  latter  found,  by  means  of  the  X-ray 
(fluoroscope),  that  the  most  important  effect  of  enteroptosis  was  to  remove 
the  support  of  the  liver  and  stomach  from  beneath  the  diaphragm.  The 
dome  of  the  diaphragm  was  thus  usually  seen  to  be  flattened 
and  to  be  situated  a  good  deal  lower  than  normal. 


Fig.  327. — The  low,  normal  and  high  hearts.  (Semi-schematic.)  I,  first  rib;  X,  tenth  rib;  VII, 
VIII,  spines  of  seventh  and  eighth  thoracic  vertebrae.  The  horizontal  line  represents  the  "xiphisternal 
line"  passing  through  the  sterno-xiphisternal  articulation.  The  small  white  arrow  represents  traction 
uixin  the  trachea.     A,  low  heart;   B,  normal  heart;   C,  high  heart. 

The  normal  summit  of  the  dome  in  quiet  expiration  is  just  above  the  level 
of  the  fifth  rib,  and  its  horizontal  shadow  just  obscures  that  of  the  tenth  rib  behind. 
Keith  finds  that  this  is  normally  about  1  cm.  above  the  ''xiphisternal  line,'' 
a  horizontal  line  representing  the  level  of  the  sternoxiphoid  articulation.  The  upper  border 
of  the  fifth  rib  at  the  junction  with  the  cartilage  is  just  at  this  level.  In  enteroptosis  Wencke- 
bach is  able  to  see  the  X-ray  shadow  of  the  origin  of  the  tenth  and  often  the  eleventh  rib 
above  the  dome  of  the  diaphragm,  and  the  latter  lies  well  below  the  xiphisternal  line. 

The  writer  finds  that  for  ordinary  purposes  the  most  convenient  landmarks  are  the 
xiphisternal  articulation  and  the  tip  of  the  spine  of  the  eighth  thoracic  vertebra,  which 
is  just  above  the  upper  border  of  the  tenth  rib.  The  xiphisternal  articula- 
tion, the  dome  of  the  diaphragm,  and  the  tip  of  the  eighth  tho- 
racic spine  are  normally  on  a  level.  In  enteroptosis  and  low  diaphragm 
the  ribs  drop  so  that  first  two  structures  are  below  the  eighth  spine,  while  with  a  high 
diaphragm  the  ribs  are  raised  so  that  they  are  above  it  (Fig.  327) . 

Effect  on  Respiration. — The  effect  of  this  low  position  of  the  diaphragm 
is  exerted  both  upon  the  respiration  and  the  heart.  The  abdominal  respira- 
tion, which  is  due  to  the  descent  of  the  liver,  is  much  diminished.  For 
when  the  dome  of  the  diaphragm  is  flattened,  shortening  of  the  diaphragm 
does  not  push  down  the  liver,  but  pulls  upon  the  lower  ribs  in  a  hori- 
zontal or  even  upward  direction.     The  effect  of  this  pull  upon  the  lower 


DISTURBANCES   OF   CARDIAC   FUNCTION.  599 

ribs  (Fig.  327,  A)  is  to  narrow  the  cross  section  of  the  thorax  (Duchenne) 
at  this  level  and  to  draw  the  epigastrium  inward,  and  thus 
by  diminishing  the  air  capacity  in  this  portion  of  the  lungs  to  decrease 
greatly  the  effect  of  inspiration  both  in  sucking  air  and  in  sucking  blood 
into  the  thorax.  This  is  the  so-called  ''paradoxical  type  of 
respiration.''  Naturally,  its  effect  is  to  diminish  the  intake  of  air 
and  thus  greatly  to  enhance  the  effect  of  any  cardiac  insufficiency. 

Effect  on  Circulation. — On  the  other  hand,  the  lessened  up-and-down 
movement  of  the  diaphragm,  coupled  with  the  relaxation  of  the  abdominal 
walls,  greatly  diminishes  the  force-pump  and  suction-pump  action  by 
which  the  blood  in  the  abdominal  veins  is  forced  onward  to  the  thorax. 
There  is,  therefore,  a  tendency  for 
the  blood  to  stagnate  in  the  abdomi- 
nal viscera.  The  venous  pressure 
becomes  low.  In  consequence,  as 
Henderson  and  the  writer  have  shown, 
the  filling  of  the  heart  is  less  complete 
and  the  systolic  output  is  diminished. 

Leonard  Hill  has  shown  that  if  a 
rabbit  is  supported  in  the  erect  posture 
with  feet  down  and  head  down,  the 
blood-pressure  falls  and  cerebral  anae- 
mia sets  in.  If  one  presses  on  the 
animal's  abdomen,  the  blood-pressure 

risjpts    flf    nnpp       Frlanp-pr    and     Hnnkpr  Fio.  328.— Radiograph  of  a  patient  with  drop- 

rises   aii  once.    ii,rianger  ana    xiooKer      pj^g  j^g^^^  (bathycardia).    (After  Brugscii  and 

found    that    when     normal     men    were         Schittenhelm.)  The  cardiac  shadow  is  separated 
,  ,1         ,  ,  .        ,  •        .  1  from   that  of  the  diaphragm  by  a  well-defined 

supported  and  kept  motionless  in  the      space. 

vertical    posture,   the    blood-pressure 

fell  {e.g.,  maximum  fell  from  120  mm.  to  103  mm.,  minimal  from  92.5  mm. 

to  86  mm.,  pulse-pressure  from  26.7  mm.  to  17  mm.'),  and  in  one  case  there 

was  "pallor,    yawning,    a    feeling    of    warmth,    faintness,    nausea,"    and 

threatened  syncope.    These  are  the  symptoms  of  arterial  anaemia  common 

in  patients  with  enteroptosis. 

The  low  position  of  the  diaphragm  exerts  another  effect  upon  the  heart. 
The  diaphragmatic  platform  on  which  it  rests  drops  away  like  a  trap-door 
and  leaves  it  suspended  from  the  great  vessels  and  vertebral  column  by 
the  aorta,  trachea,  mediastinum,  and  fasciae.  The  heart  thus  lies  in  the 
longitudinal  axis  of  the  body;  and,  in  systole,  the  apex  can  be  seen  to  rise 
and  to  pull  down  on  the  trachea  instead  of  moving  inward.  As  Osier  and 
Wenckebach  have  shown,  a  tracheal  tug  may  often  be  felt  and  this 
may  lead  to  a  mistaken  diagnosis  of  aneurism.  However, 
this  error  may  be  obviated  when  the  enteroptosis  is  taken  into  considera- 
tion, and  especially  when  the  tug  diminishes  upon  pressing  the  liver  upward 
and  inward. 

Moreover,  when  the  low  diaphragm  descends  in  inspiration  it  exerts 
further  traction  upon  the  mediastinum  and  thus  upon  the  aorta  as  well 
as  upon  the  great  veins,  thus  bringing  about  an  inspiratory  diminution 


The  fall  in  pulse-pressure  denotes  diminished  systolic  output. 


600  DISEASES   OF  THE   HEART   AND    AORTA. 

or  dropping  of  the  pulse-beats  (pulsus  paradoxus),  exactly 
like  that  occurring  in  pericarditis,  which  the  appearance  of  the  patient 
may  suggest. 

Physical  Signs. — The  upper  border  of  cardiac  dulness  in  these  cases 
does  not  usually  extend  above  the  third  rib.  The  total  area  and  the  area 
of  the  cardiac  shadow  are  usually  diminished  and  the  area  of  flatness  com- 
pletely obhterated.  The  attachments  of  the  heart  have  reverted  to  the 
embryonic  type,  and  that  organ  is  suspended  by  the  elongated  pericardiac 
Hgament.  The  a  p  e  x  is  usually  inside  the  mammillary  line.  In  extreme 
cases  the  right  ventricle  is  seen  to  beat  in  the  epigastrium;  but  this  often 
signifies  only  a  dilatation  of  that  chamber.  The  sounds  are  usually  clear, 
but  either  sound  may  be  redupHcated.  There  is  usually  a  soft  systolic 
murmur  of  accidental  type  over  the  area  of  the  right  ventricle,  or  occa- 
sionally at  the  apex. 

The  abdomen  is  often  flat,  and  usually  shows  marked  linese 
albicantes.  The  disappearance  of  subcutaneous  fat  makes  the  walls  flabby 
and  the  viscera  are  easy  to  palpate.  The  liver  can  almost  always  be  felt 
when  the  patient  is  sitting  or  standing.  The  kidneys  are  usually  palpa- 
ble and  movable.  When  the  patient  stands,  the  viscera  gravitate  to  the 
hypogastrium,  where  a  fulness  is  seen,  giving  the  abdomen  the  profile  of 
an  interrogation  point  turned  upside  down  (i,). 

Pathogenesis. — Enteroptosis  is  far  more  common  in  women  than  in 
men,  owing  to  the  stretching  of  the  abdominal  muscles  and  relaxation  of 
the  perineal  floor  in  pregnancy  and  labor.  Hence  it  occurs  more  frequently 
in  women  who  have  not  remained  in  bed  long  enough  during  the  puerperium. 
Nevertheless,  it  is  also  common  in  single  women  and  in  men  whose  abdom- 
inal muscles  are  atonic  from  lack  of  exercise,  or  in  persons  who  from  any 
cause  have  rapidly  lost  weight.  The  rapid  disappearance  of  the  intra- 
abdominal fat  uncompensated  by  contraction  of  the  abdominal  muscles 
takes  away  the  support  from  the  liver  and  facilitates  the  occurrence  of 
enteroptosis.  Indeed  this  latter  factor  is  often  more  important  than  the 
muscular  element,  and  it  is  not  uncommon  to  find  most  typical  examples 
of  enteroptosis  in  thin  persons  whose  abdominal  walls  are  not  abnormally 
flaccid. 

Tight  lacing,  as  well  as  causing  atony  of  the  abdominal  walls,  causes 
the  viscera  to  tug  at  their  ligamentous  moorings  and  finally  to  stretch 
them,  and  thus  bring  on  an  enteroptosis.  However,  while  the  corset  is 
being  worn  it  pushes  the  liver  and  diaphragm  up,  the  pelvic  organs  down. 
The  typical  corset  heart  is  the  high  heart  and  not  the  low  heart  (see 
page  327,  C).  It  is  only  when  the  corset  is  taken  off  that  the  heart  and 
abdominal  organs  drop. 

Treatment. — The  treatment  follows  from  the  mechanical  conditions. 
It  is  all-important  to  push  up  the  liver.  Fr.  Glenard,  who  first  described 
enteroptosis,  showed  that  symptoms  were  relieved  by  merely  pressing  up- 
ward on  the  abdomen  with  the  hand  (just  as  in  Leonard  Hill's  rabbit  experi- 
ment), and  hence  one  of  the  oldest  forms  of  treatment  is  the  tightly  fitting 
abdominal  binder.  A  specially  made  corset  arranged  so  as  to  bring  an 
upward  pressure  upon  all  the  structures  befow  the  costal  margin  gives 
excellent  results,  especially  when  supplemented  by  pads  over  the  kidneys. 


DISTURBANCES   OF   CARDIAC   FUNCTION.  601 

Probably  the  best  form  is  an  adjustable  air  cushion  resting  upon  an  alumi- 
num plate  that  is  strapped  to  the  abdomen  (Wenckebach).  For  a  time 
the  attention  of  physicians  had  been  directed  to  the  individual  organ, 
especially  the  kidneys,  and  these  organs  were  sutured  into  place.  But 
experience  has  shown  that  this  only  remedies  a  small  part  of  the  trouble 
and  does  not  remove  the  real  cause. 

The  only  method  of  real  physiological  therapy  is  one  which  will  at 
once  give  support  to  the  viscera  within  the  abdomen  and  also  restore  the 
tonic  contraction  of  the  abdominal  wall.  This  can  be  accomplished  by 
accumulation  of  fat  and  by  exercise.  The  former  procedure 
is  the  one  to  be  attempted  first.  If  the  patient  can  be  kept  at  absolute 
rest  in  bed  and  overfed  with  a  diet  containing  about 
3500  or  4000  calories  in  twenty-four  hours,  a  good  deal  of  fat  may 
be  accumulated  in  about  six  weeks.  The  principal  addition  to  the  diet 
should  be  olive  oil  (15  to  25  c.c.  three  times  a  day  =  about  500  calories 
per  day  or  about  60  Gm.  (2  oz.)  of  adipose  tissue).  This  can  he  taken 
between  meals,  pure  or  flavored  with  a  little  lemon,  sherry,  brandy,  etc., 
to  suit  the  palate.  It  is  most  important  that  the  patient's  digestion  should 
not  be  disturbed  by  it.  Salads  with  dressing,  thick  soups,  and  cereals 
(especially  with  cream)  should  be  given  in  as  large  quantities  as  the  patient 
will  take,  and  she  should  be  encouraged  to  drink  milk  instead  of  water. 
Butter  and  cheese  are  also  valuable  additions  to  the  diet  when  the  patient 
can  be  made  to  take  them  in  liberal  amounts.  Cakes,  sweets,  and  even 
puddings  fall  into  the  same  category,  provided  digestion  is  perfect.  She 
should  receive  milk  or  cocoa  between  meals  and  before  going  to  sleep  at 
night.  In  short,  every  means  should  be  adopted  to  overfeed  the  patient. 
On  the  other  hand,  it  must  be  remembered  that  if  her  digestion  be  spoiled 
in  the  process,  it  will  be  impossible  to  secure  a  permanent  gain  in  weight, 
so  that  the  process  must  be  begun  gradually  and  the  patient's  appetite 
should  be  stimulated  to  keep  pace  with  the  diet. 

In  order  that  the  fat  should  be  deposited  in  the  places  where  it  will 
give  the  most  support  {i.e.,  the  retroperitoneal  tissue  and  gastro hepatic 
omentum),  the  patient  should  be  made  to  lie  with  a  pillow  under  the  small 
of  the  back  for  as  many  hours  as  possible. 

The  result  of  the  rest  and  overfeeding  treatment,  supplemented  by 
careful  bandaging,  is  most  gratifying.  With  the  return  of  intra-abdom- 
inal fat  the  patients  usually  improve  in  health  and  spirits,  symptoms  sub- 
side, and  the  element  of  cardiac  weakness  may  entirely  disappear.  The 
patient's  confidence  in  herself  (or  himself)  returns  and  the  neurasthenia 
subsides. 

Case  of  Enteroptosis. 

The  following  case,  under  the  writer's  care  in  the  Johns  Hopkins  Hospital  Dispensary, 
illustrates  the  course  of  the  condition  and  the  excellent  results  obtainable  by  treatment. 

Mrs.  Agnes  L.,  aged  31,  first  seen  Feb.  19,  1909.  Complains  of  loss  of  strength, 
weakness,  and  palpitation,  especially  on  exertion.  She  is  nervous 
and   readily   exhausted.     Has  had  no  swelling  of  the  feet. 

Family  history  negative.  Patient  was  always  healthy,  but  has  had  diphtheria  and 
is  subject  to  sore  throat.  Chlorosis  at  16.  Bowels  constipated.  Menstruation  regular 
but  painful.  She  has  had  two  children  but  no  miscarriages.  Drinks  coffee  and  tea  in 
moderation. 


602 


DISEASES   OF  THE   HEART    AND    AORTA. 


Present  trouble  dates  from  birth  of  last  child  four  years  ago.  She  feels 
tired  all  the  time  and  is  subject  to  weakness  and  palpitation  after  exertion.  She  sleeps 
well,  however.  Her  feet  are  never  swollen.  Two  years  ago  she  was  treated  by  another 
physician  for  the  same  trouble,  which  was  then  diagnosed  neurasthenia.  She  was  overfed 
and  made  to  lie  down  every  day.  Gained  weight  and  improved  somewhat,  but  has  lost 
weight  since  then. 

Physical  examination  shows  a  fairly  nourished  woman,  tall  and  sparely 
built.  Her  eyes  and  cheeks  are  sunken,  and  expression  is  one  of  depression.  Her  color 
is  pale,  but  the  haemoglobin  is  90  per  cent.  Thyroid  is  not  enlarged.  No  glandular  enlarge- 
ment. Thorax  is  long  and  flat  and 
held  in  the  position  of  expiration.  Costal  angle 
is  very  acute.  There  are  a  few  rales  at  the 
left  apex  (which  were  not  present  on  subse- 
quent examinations).  The  upper  border  of 
cardiac  dulness  begins  at  the  third  rib  and 
extends  in  the  fifth  interspace  to  the  left 
mammillary  line  and  in  the  fourth  30  cm.  to 
the  right  of  the  midline.  Owing  to  the  form 
of  the  patient's  chest,  however,  the  fifth  left 
interspace  is  situated  at  a  lower  level  (referred 
to  the  spine)  than  is  normal.  The  cervico- 
xiphoid  distance  is  long.  Heart  sounds  are 
clear  and  pulse  is  regular. 

Abdomen  . —  The  liver  extends  below 
the  costal  margin.  There  is  marked  gastrop- 
tosis,  the  stomach  Ijing  below  the  umbilicus. 
Both  kidneys  palpable.    Genitalia  negative. 

Extremities.  —  Sensation  and  re- 
flexes normal. 

Patient  was  given  an  abdominal 
bandage  and  encouraged  to  full  diet, 
especially  rich  in  butter,  milk,  eggs,  and  salad. 
Besides  this  one  tablespoonful  of  olive  oil 
three  times  a  day.  She  was  made  to  rest 
and  lie  down  several  hours  a  day  with  a 
pillow  under  the  small  of  her 
back  to  favor  deposition  of  perirenal  fat. 
Within  an  hour  after  the  abdominal  binder  was  first  put  on 
her  condition  was  markedly  improved,  her  expression  was  brighter,  and 
she  felt  more  active.  The  patient,  however,  still  stood  with  stooping  shoulders,  which 
caused  the  chest  to  continue  in  the  position  of  expiration  and  allowed  the  heart  to  hang 
low.  This  position  was  improved  by  the  use  of  shoulder  braces.  The  patient's  condition 
and  strength  steadily  improved  and  her  cardiac  symptoms  had  entirely  disappeared  after  the 
abdominal  bandage  was  put  on.  The  gain  in  weight  during  three  months  was  only  3^  pounds. 


Fig.  329. — Photograph  of  a  patient  with  en- 
teroptosis.  The  upper  border  of  cardiac  dul- 
ness begins  at  the  third  rib  (III);  the  heart  is 
small  and  lies  vertically.  The  liver  is  low  and 
palpable. 


Case  of  Entergptosis  Simulating  Aneurism  of  the  Descending  Aorta. 

P.  R.,  a  wool  sorter,  aged  42,  came  to  the  Johns  Hopkins  Hospital  Dispensary  on 
March  5,  1909,  complaining  of  a  drawing  pain  in  both  sides  and  in  the  epi- 
gastrium. The  family  history  and  personal  history  were  negative.  The  patient  denies 
lues,  but  has  had  to  lift  heavy  sacks  in  his  work.  His  pain  began  about  six  weeks  before 
admission  while  he  was  at  work  and  was  accompanied  by  palpitation,  and  it  has 
continued  since  then. 

The  patient  was  a  well-nourished  man  of  good  color.  The  left  pupil  was 
larger  than  the  right,  but  both  reacted  to  light  and  accommodation.  The  thorax 
was  long  and  there  was  a  slight  funnel  breast.  The  lungs  were  clear  on  percussion  and 
auscultation.  The  area  of  cardiac  dulness  was  slightly  smaller  than  normal;  dulness 
began  above  at  the  lower  border  of  the  third  rib,  extended  7.5  cm.  to  the  left  in  the  fifth 
left  interspace  and  2.5  cm.  to  the  right  of  the  midline.  The  heart  moved  6  cm.  on 
change  of  position.    The  apex  is  3  cm.  below  the  xiphisternal  line.    The  left    radial 


DISTURBANCES   OF   CARDIAC   FUNCTION.  603 

pulse  was  slightly  smaller  than  the  right.  There  was  well-marked  pul- 
sation in  the  epigastrium,  and  the  liver  was  well  seen  and  readily  felt 
below  the  costal  margin.  There  was  a  well-marked  tracheal  tug 
which  diminished  when  the  liver  was  pushed  upwards  with 
the    hand. 

The  fluoroscopic  examination  by  Dr.  Baetjer  showed  that  the  aorta  was  clear.  An 
abdominal  binder  was  applied.  The  abdominal  pains  and  palpitation  ceased  and  the 
tracheal  tug  diminished  markedly.  The  patient  was  able  to  continue  work  without  dis- 
comfort.   His  pains  have  been  absent  for  over  a  year. 

LOW    HEART    WITHOUT    ENTEROPTOSIS    (baTHYCARDIa). 

There  is  another  type  of  long,  flat-chested  individuals  in  whom,  al- 
though there  is  no  enteroptosis,  the  diaphragm  is  low.  The  dome  of  the 
diaphragm  is  not  flat,  but  is  well  arched.  The  insertion  of  the  diaphragm 
may  be  somewhat  lower,  and  the  length  of  the  thoracic  cage,  which  is  held 
in  the  position  of  expiration,  is  considerably  greater  than  normal  (Fig. 
327,  A).  As  a  result  of  this  lengthening  of  the  thorax,  the  distance  from 
the  structures  upon  which  the  heart  hangs  (aorta,  trachea,  mediastinum) 
to  the  diaphragm,  which  supports  it,  is  lengthened,  and  just  as  in  enterop- 
tosis the  heart  hangs  free  above  the  diaphragm.  It  is  therefore  termed 
the  "hanging  heart"  or  "dropping  heart."  It  pulls  upon  the  trachea  in 
systole  and  causes  a  tracheal  tug.  It  pulls  upon  the  aorta  in  inspiration 
and  causes  a  pulsus  paradoxus.  The  interference  with  cardiac  filling  and 
with  the  abdominal  circulation  gives  rise  to  about  the  same  symptoms 
of  cardiac  weakness  as  are  encountered  in  enteroptosis,  though  often  to 
a  less  marked  degree. 

The  diagnosis  is  usually  best  made  with  the  fluoroscope;  for  the  pres- 
ence of  a  mild  brachial  impulse  and  pulsus  parado.xus  may  cause  the  con- 
dition to  be  mistaken  for  either  aneurism  or  mediastinitis.  There  may 
even  be  a  slight  tugging  on  the  low  diaphragm  (Broadbent's  sign)  at  the 
depths  of  respiration.  It  is  extremely  difficult  to  exclude  mediastino- 
pericarditis  in  many  cases  in  which  the  palpitation,  pallor,  fatigue,  short- 
ness of  breath,  paradoxical  pulse,  etc.,  are  intense.  In  some  cases  with 
reduplicated  first  sound  mitral  stenosis  may  be  thought  of.  Absence  of 
hypertrophy  of  the  left  ventricle  (cardiac  dulness  inside  mammillary  line) 
should  exclude  organic  mitral  insufficiency  even  in  the  presence  of  a  sys- 
tolic murmur.    The  diagnosis  is  made  chiefly  on  fluoroscopic  examination. 

Treatment. — As  the  condition  is  due  to  the  low  diaphragm,  just  as  in 
actual  enteroptosis,  the  chief  indication  is  to  raise  the  diaphragm.  In 
bringing  this  about  with  normal  abdominal  walls  a  bandage  is  of  some  avail, 
but  fattening  is  not  successful. 

On  the  other  hand,  the  obliquity  of  the  ribs  is  also  at  fault,  and  this 
can  be  corrected  by  training  the  patient  to  take  deep  inspirations  and  to 
stand  with  his  shoulders  and  hips  thrown  back. 

HIGH    DIAPHRAGM. 

The  exact  opposite  condition,  that  in  which  the  diaphragm  is  so  high 
that  the  heart  is  placed  in  a  position  in  which  it  works  at  a  disadvantage 
(probably  by  interference  with  venous  inflow),  is  found  in  fat  persons,  in 
many  dyspeptics  with  flatulence,  in  emphysema,  and  in  women  as  a  result 


604  DISEASES   OF  THE   HEART   AND    AORTA. 

of  tight  lacing.  In  the  first  three  conditions  there  is  diminished  respiratory 
movement,  especially  the  costal  movements,  since  the  ribs  in  most  cases 
are  held  in  the  position  of  expiration  and  the  possible  excursion  thus  dimin- 
ished; while  in  persons  who  lace  tightly  abdominal  respiration  is  impeded 
and  the  respiration  is  mainly  costal.  In  these  cases  the  heart  is  raised  by 
the  diaphragm,  especially  in  inspiration,  and  thus  comes  to  lie  more  trans- 
versely to  the  axis  of  the  body.  In  such  persons  the  xiphisternal  articula- 
tion lies  above  the  level  of  the  eighth  thoracic  spine,  the  diaphragm  shadow, 
according  to  Wenckebach,  obscuring  the  ninth  and  tenth  ribs.  The  apex 
lies  in  the  fourth  interspace  outside  the  mammillary  line,  often  leading 
to  the  suspicion  of  valvular  lesion  or  myocarditis. 

This  pushing  up  of  the  heart  tends  to  impede  the  heart's  action  and 
to  produce  fall  of  arterial  pressure,  as  was  first  shown  by  v.  Frey  and  Krehl 
in  1890. 

The  clinical  result  of  these  conditions  is  to  produce  a  syndrome  not 
unlike  that  of  the  exactly  opposite  conditions,  "cardioptosis"  and  "drop- 
ping heart," — i.e.,  a  diminished  cardiac  filling, — and  is  undoubtedly  in  a 
large  measure  responsible  for  many  of  the  symptoms  of  the  "heart  of 
obesity"  and  of  indigestion. 

Treatment  must  be  directed  to  the  cause, — regulation  of  diet  for  the 
fat  and  dyspeptic,  loosening  of  the  corset  for  the  woman  who  laces.  How- 
ever, the  latter  should  be  done  gradually  enough  to  give  the  abdominal 
walls  time  to  adjust  themselves,  lest  a  true  splanchnoptosis  replace  it. 


REFLEX    CARDIAC    DISTURBANCES. 

GASTRO-INTESTINAL. 

Patients  with  chronic  gastro-intestinal  disturbances  often  come  to 
consult  the  physician  for  the  cardiac  symptoms  which  these  bring  about, 
— namely,  palpitation,  pain  in  the  region  of  the  heart,  tachycardia,  and 
often  irregularity  of  the  pulse, — symptoms  which  are  all  more  deeply 
impressed  on  the  patient's  mind  than  are  the  heart-burn  and  belching  from 
the  underlying  indigestion. 

As  has  been  seen  in  connection  with  angina  pectoris,  gastric  disturb- 
ances may  cause  cardiac  symptoms.  The  motor  disturbances  (arrhythmia, 
tachycardia,  etc.)  are  in  a  large  part  due  to  the  spread  of  stimuli  from 
the  gastric  branches  of  the  vagus  to  the  cardiac,  while  the  sensory  symp- 
toms are  due  in  part  to  false  reference  of  impressions,  in  part  to  a 
similar  spreading  of  stimuli,  and  in  part  to  an  associated  hyperaestheria  of 
these  branches  of  the  vagus. 

The  chief  irritants  are  butyric  and  lactic  acids  (acid  fermentation), 
excess  of  hydrochloric  acid,  and  the  gases  of  fermentation, — COj  (40  per 
cent,  in  the  absence  of  HCl),  Hj,  Nj,  O^,  HjS,  and  often  CH^  (inflammable) 
in  butyric  acid  fermentation  (Hoppe-Seyler). 

Air  Swallowing. — One  of  the  most  important  factors  in  pseudocardiac 
dyspepsia  is  air  swallowing.  As  Wyllie  has  shown,  it  is  extremely 
common  for  persons  suffering  from  slight  gastric  discomfort  to  find  them- 
selves relieved  by  belching.    As  a  result  they  seek  further  relief  by  forcing 


DISTURBANCES   OF   CARDIAC   FUNCTION.  605 

themselves  to  belch.  The  forced  belching  gives  only  momentary  relief, 
but  aggravates  the  discomfort,  giving  rise  to  a  familiar  sensation  of  an 
object  lying  just  behind  the  larynx.  They  belch  again  to  remove  it,  and 
the  belching  is  thus  continued  indefinitely,  always  accompanied  by  a  cer- 
tain discomfort  and  often  by  a  loud  noise. 

Mechanism  of  Acrophagia. — Wyllie  and  others  have  shown  that  the  mechanism 
of  involuntary  and  voluntary  belching  is  quite  different.  In  the  former 
case  an  excess  of  the  gases  of  fermentation  is  regurgitated  from  the  stomach,  and  this 
can  occur  only  when  there  is  an  excess  of  gas.  In  the  latter  case  the  patient  first  swal- 
lows or  gulps  the  air  by  placing  the  tongue  against  the  roof  of  the  mouth  (in  the  position  of 
pronouncing  the  consonant  "  T"  and  then  exerting  a  deep  inspiration.  These  movements 
force  the  air  into  the  oesophagus.  It  remains  there  an  instant,  and  may  then  be  either 
swallowed  or  expelled  by  a  forced  expiration  with  the  glottis  closed,  causing  the  loud 
noise  of  belching  as  it  forces  apart  the  vocal  cords  and  pushes  up  the  epiglottis.  Most 
often  part  of  the  air  is  swallowed  and  part  regurgitated,  and  a  few  bubbles  of  air  remain 
in  the  oesophagus  most  of  the  time,  giving  rise  not  only  to  the  feeling  of  discomfort  but 
often  to  reflex  cardiac  disturbances.  Wyllie  calls  attention  to  the  fact  that  air  gulping 
occurs  not  only  in  man  but  also  in  horses  and  cattle,  where  the  condition  is  known  as 
"  wind  colic  "  and  "  hoven,"  which  often  becomes  so  severe  that  it  may  cause  the  death 
of  the  animal.  The  symptoms  are  "  difficult  breathing,  bloodshot  eyes,  red  mucous 
membrane,  loud  tumultuous  heart-beat,  trembling  of  front  legs,  etc."  This 
can  be  brought  about  in  dogs  by  inflating  either  .stomach  or  intestines  with  air  under 
pressure,  paralysis  and  heart-failure  resulting.  Wyllie  believes  that  the  condition  is  still 
more  common  in  infants  and  in  children,  and  thinks  that  it  is  responsible  not  only  for 
wind  colic  but  for  certain  cases  of  death  with  abdominal  distention. 

Palpitation  when  patients  are  quiet  may  be  more  striking  than  actual  shortness  of 
breath  on  moderate  exertion  (imless  anaemia  is  also  present).  But  this  is  not  an  invariable 
rule,  for  on  account  of  the  high  diaphragm  of  flatulence,  the  intensity  of  the  cardiac  dis- 
comfort, or,  on  the  other  hand,  the  habitual  weakness  of  the  patient's  muscles,  there  may 
be  actual  cardiac  weakness  as  well. 

The  treatment  of  air  gulping  is  of  the  greatest  importance.  Wyllie 
states  that  this  troublesome  habit  can  be  promptly  overcome  by  keeping 
the  mouth  open.  For  persons  who  swallow  air  in  their  sleep,  a  gag  or  cork 
has  to  be  tied  in  the  mouth.  This  method  is  in  general  use  among  veterinary 
surgeons  and  is  uniformly  successful.  It  is  evident,  therefore,  that  the 
diagnosis  of  air  swallowing  must  be  carefully  made.  In  many  cases  this 
may  be  done  by  getting  the  patient  to  show  you  how  she  usually  belches, 
the  voluntary  procedure  indicating  the  nature  of  the  process.  In  doubtful 
cases  it  may  be  necessary  to  analyze  the  gas  by  Hoppe-Seyler's  method; 
but,  as  Wyllie  remarks,  the  diagnosis  is  best  made  ex  juvantibus,  by  cessa- 
tion of  the  condition  when  the  mouth  is  kept  open.  The  possibility  of 
unconscious  quiet  air  swallowing  in  other  cases  of  flatulence  must  also  be 
borne  in  mind. 

Constipation. — An  accumulation  of  fecal  matter  is  also  a  very  common 
cause  of  cardiac  symptoms.  Extrasystoles  are  usually  more  common 
when  the  patients  are  constipated.  Kuthan  has  also  seen  patients  in 
whom  attacks  of  angina  pectoris  occurred  regularly  during  periods 
of  constipation  and  disappeared  when  the  bowels  were  kept  open.  These 
symptoms  are  produced  partly  by  the  lifting  of  the  diaphragm  and  per- 
haps also  in  part  by  the  chemical  action  of  indol,  skatol  (Russell, 
Herter),  and  other  fermentation  products.  These  substances  may  act 
directly  upon  the  intestinal  nerve  endings  or  upon  the  heart  muscle  and 


606  DISEASES   OF  THE   HEART   AND    AORTA. 

cardiac  nerves  after  absorption  into  the  general  circulation  (as  assumed 
by  McCaskey).  It  must  be  admitted  that  the  action  of  such  products 
is  not  very  well  known. 

Apart  from  the  general  methods,  treatment  of  the  cardiac  symptoms 
is  best  accomplished  by  treating  the  gastric  condition  with  appropriate 
diet,  lavage,  galvanization  (8  to  12  milliamperes),  and  faradization  of  the 
stomach,  etc.  The  bowels  should  be  kept  open.  The  various  forms  of 
fermented  milk  containing  lactic  acid  (buttermilk,  kephyr,  etc.)  as  well 
as  the  preparations  of  lactic  acid  bacilli  are  often  of  benefit  in  the  treat- 
ment of  intestinal  fermentation. 

Treatment  of  the  constipation  which  is  often  present  should  consist 
of  free  purgation  with  Epsom  salts,  followed  by  a  course  in  cascara,  hydro- 
therapy, abdominal  exercise,  and  a  diet  rich  in  fat,  coarse  foods,  and  in 
liquids.  The  most  important  feature  is  forcing  the  patient  to  defecate  at 
regular  hours  and  at  no  other  times. 

REFLEXES  FROM  THE  SEXUAL  ORGANS. 

Practically  all  the  disturbances  of  the  sexual  organs  are  accompanied 
by  the  pseudocardiac  syndrome.  It  occurs  in  both  male  and  female  after 
sexual  excesses  and  organic  diseases. 

MALE    SEXUAL    ORGANS. 

In  men  gonorrhoea,  prostatitis,  and  especially  masturbation  are  among 
the  first  conditions  to  be  thought  of  when  a  patient  presents  himself  with 
these  symptoms.  Curschmann  and  Bachus  have  especially  called  attention 
to  the  latter  condition  and  have  found  that  masturbation  may  even  lead 
to  cardiac  hypertrophy.  Bachus  has  made  the  very  significant  observa- 
tion that  in  many  of  his  masturbators  the  thyroid  glands  were 
somewhat  enlarged,  so  that  he  believed  that  the  abnormal  sexual 
activity  might  have  led  to  a  secondary  over-activity 
of  the  thyroid.  (Perhaps  this  may  occur  through  the  action  of  a 
hormone  in  the  testicles,  seminal  vesicles,  or  prostate.)  At  all  events, 
since  this  organ  may  be  affected  reflexly,  the  secondary  activity  of  the 
thyroid  is  to  be  thought  of  in  all  cases  of  pseudocardiac  disease  of  sexual 
or  of  purely  nervous  origin.  It  is  also  possible  that  the  prostate  gland 
may  have  an  internal  secretion  of  similar  character. 

The  diagnosis  must  be  made  from  the  history,  as  well  as  from  a  careful 
physical  examination  in  which  the  mouth  of  the  urethra  is  especially  exam- 
ined, and  careful  palpation  of  the  prostate  and  prostatic  secretion. 

Treatment  is  directed  mainly  to  the  primary  condition,  but  the  bro- 
mides should  be  used  somewhat  more  freely  in  sexual  disturbances  than 
in  the  other  conditions. 

FEMALE. 

In  women  the  pseudocardiac  disturbances  are  not  only  more  common 
but  more  severe  than  is  usual  in  men.  Palpitation,  with  tachycardia  and 
weakness,  is  very  common  at  the  age  of  puberty  and  is  practically  universal 
in  chlorosis  which  is  then  so  common. 


DISTURBANCES   OF   CARDIAC   FUNCTION.  607 

In  young  and  healthy  married  women  Kisch  has  found  that  attacks 
of  palpitation  with  rapid  pulse  and  dyspnoea  may  occur — 

1.  As  the  result  of  sexual  excesses  in  women  whose  sexual  desire  is  very  keen. 

2.  After  attempted  coitus  when  vaginismus  is  present  (cured  by  operation  upon  the 

vagina). 

3.  In  women  who  have  practised  coitus  interruptus  for  a  long  time  without  attaining 

sexual  satisfaction. 

Kisch  believes  that  in  general  coitus  stimulates  the  cardiac  nerves 
in  proportion  to  the  intensity  of  the  orgasm.  Masturbation,  on  the  other 
hand,  has  a  much  less  intense  effect  on  women  than  on  men  (Kelly),  and 
is  rarely  responsible  for  cardiac  disturbances. 

Veit  calls  attention  to  the  fact  that  asthmatic  attacks  from 
cardiac  insufficiency  constitute  an  early  symptom  of 
myoma.  He  believes  that  these  arise  in  the  early  stages  of  brown 
atrophy  and  cardiac  obesity,  as  these  lesions  have  been  found  by  Lehmann 
and  Strassman  and  also  by  Fleck  in  40  per  cent,  of  all  cases  of  myoma.' 
Kelly  and  Cullen,  however,  deny  that  myomata  in 
themselves  are  associated  with  any  cardiac  disturb- 
ances except  those  due  to  the  anaemia  which  is  pres- 
ent. In  a  very  careful  study  of  1428  cases  of  myoma  they  found  that 
"In  the  majority  of  cases  (with  cardiac  manifestations,  92)  an  apical  sys- 
tolic murmur  was  detected.  This  murmur  was  usually  very  soft  in  character. 
In  some  it  was  limited  to  the  apex,  but  in  others  it  could  be  traced  to  the 
axilla  and  in  some  patients  to  the  base  of  the  heart."  In  nearly  all  the 
cases  (92)  in  which  cardiac  lesions  were  present,  the  patient  gave  a  history 
of  menorrhagia,  often  associated  with  intermenstrual  bleeding.  These 
patients,  as  a  rule,  stood  the  anaesthetic  well  and  in 
a  comparatively  short  time  they  had  gained  much  in  strength  and  their 
cardiac  murmurs  had  disappeared.  Some  authorities  claim  that  the  myoma 
in  itself  brings  about  cardiac  changes.  If  such  were  the  case,  then  the 
larger  the  myoma  the  more  pronounced  should  be  the  cardiac  murmurs. 
This  has  not  been  our  experience.  The  largest  tremors  have  not  been 
associated  with  any  cardiac  symptoms,  but  the  heart  complications  have 
almost  invariably  been  associated  with  copious  bleeding  from  the  uterus 
{i.e.,  submucous  myomata). 

"  Most  of  the  murmurs  noted  in  our  cases  were  at  the  time  considered 
to  be  functional."  (Cullen.)  That  there  is  little  danger  from  functional 
impairment  of  the  heart  is  shown  by  the  fact  that  Kelly  and  Cullen's  mor- 
tality in  their  last  240  cases  of  myoma  was  less  than  1  per  cent. 

Lenhartz  has  found  that  cardiac  symptoms  are  almost  always  more 
frequent  during  the  week  preceding  the  menstrual  flow.  They 
are  also  more  frequent  as  the  climacteric  is  approached,  an  angioneurosis 
(flushing)  with  palpitation  and  more  or  less  tachycardia  being  universal. 
Strassman  and  Lehmann  have  called  attention  to  the  similarity  between 
these  phenomena  in  ovarian  secretion  and  those  of  the  thyroid  gland, 
and,  as  has  been  stated,  the  thyroid  varies  in  size  with  the  changes  in  ova- 
rian activity.     Leo  Loeb,  Starling,  and  others  have  shown  that  this  is  due 

*  In  34.6  per  cent,  of  Fleck's  cases  there  was  no  anjemia. 


G08  DISEASES   OF   THE    HEART    AND    AORTA. 

to  the  action  of  a  hormone  arising  in  the  ovaries  and  especially  in  the  corpus 
luteum,  which  acts  upon  the  uterus,  mammary  glands,  and  thyroid.  No 
doubt  it  also  has  some  action  upon  the  heart,  but  this  is  still  obscure,  and 
it  is  difficult  to  determine  how  much  of  the  effect  is  due  to  the  ovarian 
secretion  itself  and  how  much  to  the  secondary  hyperthyroidism. 

Prognosis  and  Therapy. — The  prognostic  importance  of  cardiac  dis- 
turbances arising  in  the  sexual  organs  varies  with  the  primary  lesion  and 
its  chronicity.  In  the  presence  of  gonorrhcEa  or  pelvic  abscesses  the  prob- 
ability of  a  metastatic  myo-  or  endocarditis  must  not  be  forgotten.  In 
the  presence  of  anaemia  the  development  of  fatty  degeneration  and  even 
of  insidious  mitral  stenosis  must  be  borne  in  mind,  while  in  the  presence 
of  myoma  myocardial  changes  which  vary  from  primary  hypertrophy  to 
a  brown  atrophy  and  cardiosclerosis  (due  chiefly  to  the  anaemia)  must  be 
thought  of.  In  masturbating  men  there  is  a  true  cardiac  hypertrophy  with 
the  usual  accompanying  changes.  These  factors  must,  therefore,  be  ex- 
cluded before  the  diagnosis  of  a  true  neurosis  is  made  and  an  unqualified 
favorable  prognosis  can  be  given. 

In  the  simple  cardioneurosis  or  pseudocardiac  sexual  disturbance 
the  cardiac  outlook  is  favorable  if  the  primary  condition  can  be  removed. 
If  not  the  prolonged  reflex  stimulation  of  the  cardiac  nerves  leads  first  to 
a  "work  hypertrophy"  and  then  probably  to  cardiac  overstrain  and  pre- 
mature cardiosclerotic  or  atrophic  changes. 

The  treatment  is  therefore  in  the  field  of  the  gynaecologist  or  genito- 
urinary specialist  and  not  in  that  of  the  internist.  Even  masturbation 
and  sexual  excesses  may  have  a  basis  in  organic  irritation  and  should  not 
be  regarded  as  entirely  psychogenic  without  examination.  These  may 
be  much  helped  by  psychotherapy,  cold  baths  in  the  morning  and  cold 
packs  at  night,  and  exercise  during  the  day.  The  psychic  effect  of  the 
treatment  will  be  greatly  enhanced  if  the  impression  is  clinched  at  once 
by  the  administration  of  potassium  or  sodium  bromide  (1  Gm.  =  gr.  xv, 
t.i.d.  and  before  going  to  bed)  disguised  in  elixir  of  calisaya  or  in  com- 
pound tincture  of  gentian  or  of  cardamom;  for  the  patient's  confidence 
in  the  outcome  is  gained  by  finding  the  abnormal  desire  to  decrease  at 
once  with  the  onset  of  treatment. 

ADENOIDS  AND  RESPIRATORY  OBSTRUCTION. 

Adenoids. — The  presence  of  adenoid  growths  in  the  nasopharynx  is  also 
of  importance,  not  only  because  they  interfere  with  the  respiratory  intake  of 
air  and  thus  bring  about  dyspnoea  on  exertion,  which  may  simulate  a  true 
cardiac  weakness,  but  also  because  attacks  of  mild  asphyxia  may  occur 
during  sleep  and  cause  the  patient  to  awaken  suddenly  with  a  severe  palpi- 
tation and  other  cardioneurotic  symptoms.  Besides  this,  during  waking 
hours  the  lesions  may  continue  to  produce  reflex  irritation  of  the  cardiac 
nerves  and  give  rise  to  cardioneurotic  symptoms  in  the  same  way  as  do 
disturbances  in  other  organs. 

Arrhythmia  of  Nasal  Origin. — A  physiological  basis  for  these  clinical 
findings  has  been  furnished  by  Frangois-Franck  (1889),  who  found  that 
an  arrhythmia  of  vagal  origin  could  be  produced  by  stimulating  the  nasal 


DISTURBANCES   OF   CARDIAC   FUNCTION.  609 

mucosa.  His  studies  have  recently  been  confirmed  by  Koblanck  and 
Roeder,  who  found  that  in  8  cases  with  arrhythmia  and  nasal  disease 
there  were  alterations  in  the  mucous  membrane  of  the  nasal  septum  in 
a  spot  opposite  the  middle  turbinate  bone.  There  were  often  nose-bleeds 
as  well.  Touching  this  spot  with  a  blunt  probe  in  man  and  animals 
produced  a  similar  arrhythmia.  No  other  area  of  nasal  mucosa 
gave  this  reflex.  The  arrhythmia  was  characterized  by  series  of  beats  with 
increasing  rapidity  interrupted  by  long  pauses,  sometimes  simulating 
extrasystolic  bigemini  (Curves  1  (man)  and  3  (rabbit),  K.  and  R.),  but  it 
could  not  be  produced  after  either  vagus  was  cut.  Stimulation  of  other 
mucous  membranes  in  this  manner  did  not  give  rise  to  such  arrhythmia. 
The  authors  showed  that  these  stimuli  are  carried  by  the  septal  branch  of 
the  trigeminus  which  lies  in  this  vicinity,  for  they  could  not  be  produced 
after  cutting  the  trigemini,  and  believe  that  they  are  carried  directly  from 
the  trigeminus  nucleus  to  that  of  the  vagus  through  the  fasciculus  longi- 
tudinalis  medialis.  With  cure  of  the  nasal  condition  the  arrhythmia  and 
allied  disturbances  disappeared. 

Cardiac  Asthma  from  Disease  of  Nasal  Septum. — Frangois-Franck  also 
showed  by  careful  graphic  methods  that  stimulation  of  the  nasal  reflex  can 
give  rise  to  cough,  laryngeal  spasm,  asthma,  and  even  a  reflex  bronchitis, 
reflexes  which  in  themselves  may  add  to  the  impression  of  a  primary 
cardiac  disturbance.  He  found  that  these  reflex  conditions  were  more 
pronounced  in  animals  with  aortic  insufficiency  than  in  normal  animals. 
The  condition  in  man  is  similar,  and  in  the  presence  of  an  organic  cardiac 
lesion  these  contributing  factors  may  play  a  role  which  determines  the 
security  of  the  cardiorespiratory  symptoms,  so  that  the  cause  of  the 
paroxysmal  dyspnoea  may  in  some  cases  have  to  be  looked  for  in  the  nose. 


TOXIC   CARDIONEUROSES. 

"TOBACCO  HEART." 

Persons  who  suffer  from  excessive  use  of  tobacco  may  be  divided  into 
three  classes: 

1.  Non-smokers  suffering  from  a  single  indulgence  (acute  tabagism  or  nicotinism). 

2.  Young  habitual  smokers,  especially  those  who  inhale  cigarette  smoke  (subacute 

nicotinism) . 

3.  Old  habitual  smokers,  especfelly  of  cigars  and  pipes,  who  suffer  from  the  patho- 

logical changes  produced  in  the  arteries  (especially  the  coronary  arteries)  and 
myocardium,  and  partly  from  the  added  effects  of  the  nicotine. 

PHYSIOLOGICAL   EFFECTS. 

The  physiological  effect  of  smoking  has  recently  been  studied  by  Lee, 
as   well   as   by   Bruce,    Miller,    and    Hooker. 

Lee  found  that  ordinary  tobacco  smoke  obtained  from  1000  Gm.  tobacco  contained 
nicotine  1.165  Gm.,  pyridine  bases  (chiefly  pyridine  and  collidine)  0.148  Gm.,  HCN  0.08 
Gm.,  NH3  0.36  Gm.,  CO  410  c.c.  The  chief  toxic  product  is  therefore  nicotine.  The 
composition  varied  considerably  with  both  the  quahty  of  the  tobacco  and  the  mode  of 
smoking.  The  greater  part  of  the  nicotine  at  the  seat  of  combustion  is  destroyed,  and  that 
39 


610  DISEASES   OF   THE   HEART    AND    AORTA. 

which  reaches  the  mouth  is  volatiHzed  by  the  hot  gases  while  passing  over  the  unburned 
area.  Accordingly  a  thick  cigar  has  the  worst  effect,  since  it  acts  as  a  chimney  leading 
the  gases  to  the  mouth,  while  in  a  thin  cigar,  "  stogie,"  or  cigarette  they  escape  into  the 
surrounding  air.  (In  cigarette  smoking  inhaling  the  smoke  more  than  compensates  for 
this  difference  in  combustion.)  In  long-stemmed  pipes  much  of  the  nicotine  condenses 
before  reaching  the  mouth. 

Lee  found  that  in  non-smokers  the  first  effect  of  smoking  a 
cigar  was  to  produce  a  rise  of  10-20  mm.  Hg  in  the  maximal  blood-pressure, 
which  was  often  associated  with  palpitation.  Within  five  minutes  after 
this  the  maximal  blood-pressure  fell  50  mm.  Hg,  and  this  fall  was  accom- 
panied by  pallor,  sweating,  weakness,  and  colicky  pains  in  the  abdomen,  as 
well  as  by  the  appearance  of  muscse  volitantes,  irregularity  and  weakness 
of  the  pulse, — or,  in  other  words,  the  symptom  complex  of  arterial  anaemia. 

In  more  habitual  smokers,  those  of  the  second  group,  a  single 
cigar  produced  only  the  rise  of  blood-pressure  and  palpitation.  The  subacute 
symptoms,  therefore,  come  on  only  as  the  result  of  excessive  indulgence. 

In  old  habitual  smokers  these  observers  found  either  no 
effect  whatever  or  only  a  slight  rise  of  pressure  resulting  from  a  strong 
cigar,  without  any  of  the  disagreeable  symptoms. 

Lee's  observations  have  been  repeated  by  Bruce,  Miller,  and  Hooker, 
who  found  that  smoking  increases  the  maximal,  minimal,  and 
pulse-pressures  in  man,  though  later  these  return  to  normal.  The 
cardiac  output,  therefore,  seems  to  be  increased  at  first,  as  Lee  had  found 
in  cats.  Bruce,  Miller,  and  Hooker  also  found  that  the  volume  of 
the  hand  always  decreased  during  smoking  (vasoconstriction), 
whereas  Lee  found  that  the  volume  of  the  cat's  intestine  also  decreased. 
It  is  probable  that  a  little  later  there  occurs,  in  man,  a  dilatation  of  the 
abdominal  vessels,  but  it  is  not  yet  certain  that  it  does  so. 

The  chief  sufferers  from  tobacco  are  the  young  cigarette  smokers  who 
inhale  the  smoke  and  thus  soon  suffer  immediately  from  the  physiological 
effects  of  the  nicotine.  They  complain  of  weakness,  giddiness, 
intense  palpitation  and  tachycardia  (from  continued  stim- 
ulation of  the  cervical  ganglion  cells) ,  and  often  of  irregularity  of 
the  heart,  which  may  be  very  distressing.  It  is  most  noticeable  that  the 
intense  sensory  disturbances  occur  without  any  motor  insufficiency  of 
the  heart.  Thus,  a  young  man  of  20  years,  an  habitual  inhaler  of  cigarette 
smoke,  recently  consulted  the  writer,  complaining  of  fatigue,  giddiness, 
muscae  volitantes,  intense  palpitation,  but,  on  further  questioning,  stated 
that  he  was  in  the  habit  of  running  a  quarter  of  a  mile  every  evening  for 
exercise,  and  after  this  exercise  he  had  neither  palpitation  nor  shortness 
of  breath!    Needless  to  say,  he  improved  at  once  after  stopping  tobacco. 

On  the  other  hand,  all  sufferers  from  nicotine  are  not  free  from  motor 
symptoms  nor  do  they  recover  so  readily.  In  many  cases  the  nicotinism 
is  supplemented  by  the  use  of  alcohol,  and  secondary  myocardial  changes, 
and  in  the  older  persons  arteriosclerotic  changes,  have  been  superinduced. 

In  the  middle-aged  smokers  the  symptoms  are  chiefly  those  of  angina 
pectoris  and  precordial  pain.  Very  commonly  this  is  a  true  angina  of  cora- 
nary  sclerosis,  but  there  is  a  certain  number  of  cases  in  which  the  unpleasant 
symptoms  completely  subside  upon  cessation  of  smoking. 


DISTURBANCES   OF   CARDIAC   FUNCTION.  611 

It  would  be  a  very  fascinating  hypothesis  to  believe  that  in  such  cases  the  effect  of 
smoking  is  to  produce  a  transitory  constriction  of  the  coronary  arteries  and  this  to  cause 
the  symptoms,  but,  on  the  contrary,  some  recent  experiments  upon  dogs,  done  under  the 
writer's  direction  by  Dr.  George  Bond,  have  shown  that  the  flow  through  the  coronary 
veins  is  actually  increased  by  smoking.'  It  is  probable,  therefore,  that  in  early  tobacco 
poisoning  at  least,  the  sensory  s5anptoms  are  due  to  stimulation  of  the  cardiac  nerves  and 
not  to  ischaemia  of  the  myocardium.  The  commonness  and  insidiousness  of  coronary 
sclerosis,  however,  render  it  difficult  to  decide  in  any  individual  case  whether  the  effect 
is  entirely  functional  or  has  also  a  basis  in  arterial  changes. 

COFFEE  AND  TEA. 

The  palpitation,  tachycardia,  and  tremor  which  result  from  over- 
indulgence in  coffee  and  tea  are  familiar  to  most  persons  from  personal 
experience.  They  often  manifest  themselves  in  chronic  forms  and  cause 
cardioneurotic  symptoms.  Precordial  pain  and  tenderness  are  quite  com- 
mon. Foote  and  Simpson,  under  D.  R.  Hooker's  direction,  have  found 
that  when  a  person  accustomed  to  coffee  takes  a  cup  of  it  there  is  a  transi- 
tory rise  in  maximal  and  minimal  blood-pressure  and  a 
slight  vasoconstriction  of  the  hand.  In  persons  unaccustomed  to 
coffee  these  changes  are  much  more  intense.  Indeed  this  partial  immunity 
to  coffee  is  very  transitory,  for  the  writer  has  found  that  after  discontinuing 
its  use  for  several  months  a  single  cupful  would  give  rise  to  palpitation, 
tachycardia,  and  insomnia,  while  a  few  months  before  and  a  few  months 
later  two  cups  could  be  taken  at  a  time  without  producing  symptoms. 

Coffee,  like  tobacco,  gives  rise  to  sensory  cardiac  symptoms  by 
increasing  the  irritability  of  the  nerves  without  causing  any  motor  insuf- 
ficiency, and  consequently  the  patients,  as  a  rule,  do  not  show  muscular 
or  cardiac  fatigue  on  exertion  in  spite  of  the  symptoms. 

Tea. — Owing  to  its  content  of  caffeine,  tea  causes  the  same  symptoms 
as  coffee,  but  is  less  extensively  used  in  large  quantities.  In  England, 
however,  similar  cases  are  occasionally  reported. 

ALCOHOL. 

Palpitation  and  the  other  symptoms  of  "cardioneurotic"  (pseudo- 
cardiac)  weakness  also  occur  in  persons  who  take  alcohol  in  quantities 
that  are  just  in  excess  of  their  tolerance,  and  the  possibility  of  this  cause 
must  be  borne  in  mind.  In  some  individuals,  as  in  Reissner's  case,  palpi- 
tation and  irregularity  may  follow  the  ingestion  of  a  single  glass  of  wine, 
without  any  symptoms  of  intoxication  setting  in.  That  these  conditions 
may  continue  without  the  patient's  recognizing  the  cause  is  a  common 
experience,  and  a  considerable  number  of  cardioneurotic  cases  result  from 
this  unintentional  over-indulgence  in  alcohol.  Women  and  young  persons 
are  more  sensitive  than  men.  The  functional  power  and  endurance  of  the 
heart  muscle  is,  moreover,  weakened  by  alcohol;  and  acute  dilatation  may 
set  in  from  comparatively  slight  exertion.  If  the  use  of  alcohol  is  long 
continued,  it  may  lead  to  fatty  and  fibrinous  myocardial  change,  but  this 
in  mild  cases  subsides  when  the  cause  is  removed. 

*  Bond  registered  the  outflow  from  tlie  coronary  veins  by  the  drop  method. 


612  DISEASES   OF   THE   HEART    AND    AORTA. 

SIMPLE   EMOTIONAL   CARDIONEUROSES. 

As  has  been  seen,  by  far  the  greatest  number  of  so-called  cardioneurotic 
cases  are  of  postural,  reflex,  or  toxic  origin.  However,  it  still  remains 
beyond  question  that  emotional  disturbances  alone,  or  in  conjunction  with 
other  conditions  which  in  themselves  are  not  sufficiently  intense  to  pro- 
duce symptoms,  may  give  rise  to  cardioneurotic  symptoms.  Palpitation 
and  even  precordial  pain  are  almost  universal  after  severe  emotional 
disturbances  and  shocks  and  during  periods  of  worry. 

The  motor  effects  are  usually  shown  by  tachycardia,  though  occa- 
sionally arrhythmias  may  occur.  This  the  writer  has  observed  upon  him- 
self on  an  occasion  of  intense  emotion,  during  which  the  pulse  became 
extremely  rapid  and  seemed  either  to  drop  an  occasional  beat  or  to  give 
rise  to  an  extrasystole.  When  the  cause  of  the  worry  was  removed,  within 
five  minutes  the  pulse  again  became  regular,  so  that  the  arrhythmia  could 
not  be  accurately  studied  nor  has  it  recurred  at  any  other  time  during  the 
four  years  that  have  elapsed. 

Similar  cases  are  found  in  the  literature  (Reissner).  In  rare  cases  an 
emotional  shock  may  cause  death,  even  when  the  heart  is  otherwise  healthy 
(Gibson),  but  the  nervous  mechanism  by  which  this  is  brought  about  is 
not  clearly  understood.  It  is  probably  a  condition  of  exaggerated  vaso- 
motor shock  arising  in  response  to  a  cortical  stimulus,  just  as  it  may 
result  from  over-stimulation  of  a  peripheral  nerve.  In  most  cases  of 
the  sort,  however,  the  heart  and  especially  the  coronary  arteries  are 
already  diseased  (see  page  281). 

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1903.     Diseases  of  the  Heart,  Lond.,  1908. 
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the  String  Galvanometer,  Quart.  J.  Exper.  Physiol.,  Lond.,  1908,  i,  243. 
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Physiol.,  Bonn,  1900,  Ixxxii,  1. 
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Verhandl.  d.  Kong.  f.  innere  Med.,  Wiesb.,  1908,  xxv,  292. 
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DISTURBANCES   OF   CARDIAC   FUNCTION.  613 

Mosse:  Demonstration  eines  Falles  von  idiopathischer  Bathycardie,  Deutsch.  med.  Wchn- 
schr.,  Leipz.,  1900,  Ver.  Beil.  266. 

Janevvay,  E.  G.:  Bathycardia,  Trans.  Asso.  Am.  Physicians,  Phila.,  1903,  xviii,  5  (also 
discussion  by  Osier). 

Keith,  A.:  The  Nature  and  Anatomy  of  Visceroptosis,  Lancet,  Lond.,  1904,  i,  551,  631, 
709,  818.  A  Method  of  Indicating  the  Position  of  the  Diaphragm  and  Estimating  the 
Degree  of  Visceroptosis,  J.  Anat.  and  Physiol.,  Lond.,  1908,  xlii,  26. 

Hill,  L.:  The  Mechanism  of  the  Circulation,  Schafer's  Text-book  of  Phsyiol.,  Edinb.  and 
Lond.,   1900,   ii,  46. 

Erlanger,  J.,  and  Hooker,  D.  R.:  An  Experimental  Study  of  Blood-pressure  and  of  Pulse- 
pressure  in  Man,  Johns  Hopkins  Hosp.  Rep.,  Baltimore,  1904,  xii,  147. 

V.  Frey,  M.,  and  Krehl,  L.:  Untersuchungen  iiber  den  Puis,  Arch.  f.  Physiol.,  Leipz., 
1890,  31. 

Hoppe-Seyler,  G.:  Zur  Kenntniss  der  Magengahrung  mit  besonderer  Berucksichtigung 
der  Magengase,  Deutsch.  Arch.  f.  klin.  Med.,  Leipz.,  1892,  1,  82. 

Wyllie,  J.:  On  Gastric  Flatulence,  Edinb.  Hosp.  Rep.,  1895,  iii,  21. 

Special  Report  on  Diseases  of  Cattle,  U.  S.  Dept.  of  Agriculture,  Washington,  1904. 

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Kuthan,  F.:  Die  Obstipation  und  ihre  Einfluss  auf  die  Herztatigkeit,  Zentralbl.  f.  innere 
Med.,  1906,  xxvi,  1076. 

Veit:  Aetiologie  und  Symptomatologie  de  Myome,  Handb.  d.  Gynakol.,  1898,  ii. 

Stra.ssmann  and  Lehmann.    Quoted  from  Fleck. 

Fleck,  G. :  Myom  und  Herzerkrankungen  in  ihren  genetischeu  Beziehungen,  Arch,  f .  Gyna- 
kol., 1904,  Ixxi,  258. 

Kelly,  H.  A.,  and  Cullen,  T.  S.:  Myomata  of  the  Uterus,  Phila.,  1909. 

V.  Rosthorn,  Lenhartz,  Link,  Schott,  Krehl,  Klemperer,  Groedel,  Janowski,  Fellner: 
Discussion  of  "  Die  Beziehungen  der  weiblichen  Geschlechtsorgane  zu  inneren  Erkran- 
kungen,  Verhandl.  d.  Kong.  f.  innere  Med.,  Wiesbaden,  1908,  xxv,  29. 

Lazarus:  Die  adenoide  Vegetationen  und  ihre  Beziehungen  zur  dilatativen  Herzschwache, 
Festschr.  f.  Leyden,  1902. 

Frangois-Franck,  Ch.  A.:  Contribution  k  I'^tude  experimentale  des  nevroses  reflexes 
d'origine  nasale,  Arch,  de  physiol.  de  I'homme  et  des  anim.,  Par.,  1889,  5e  Ser.  i,  538. 

Koblank  and  Roeder,  H. :  Experimentalle  Untersuchungen  zur  reflektorischen  Herzarhyth- 
mie.  Arch.  f.  d.  ges.  Physiol.,  Bonn,  1908,  cxxv,  377. 

Lee,  W.  E.:  The  Action  of  Tobacco  Smoke,  with  Special  Reference  to  Arterial  Pressure  and 
Degeneration,  Quart.  J.  Exper.  Physiol.,  Lond.,  1908,  i,  335. 

Bruce,  Miller,  and  Hooker:  The  Effect  of  Smoking  on  the  Blood-pressures  and  the  Volume 
of  the  Hand,  Am.  J.  Physiol.,  Bost.,  1909. 

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Deutsch.  Arch.  f.  klin.  Med.,  Leipz.,  1907,  Ixxxix,  432. 


INDEX 


Abdominal  aorta,  aneurism  of,  550 
Abdominal  pain  from  distended  liver,  159 

in  tricuspid  insufficiency,  400 
Abscess  of  heart-muscle,  226 
Absolute  arrhythmia,  effect  of  digitalis  in,  78 

(see  also  Arrhythmia) 
Acapnia,  Cheyne-Stokes  breathing  from,  152 

in  shock  and  fevers,  31 
Accelerations,  reflex,  62 
Accessory  heart-sounds,  104 
Accidental  murmurs  in  splanchnoptosis,  600 
Acetonitrile  test  for  hyperthyroidism,  578 
Aconite,  185 

pharmacological  action  of,  185 
therapeutic  use  of,  185 
with  digitalis,  186 
Aconitin,  185 
Acrocyanosis,  274 
Acroparaesthesia,  274 

Adams-Stokes    disease    (see    also    Adams- 
Stokes    syndrome;    Heart- 
block),  460 
auricular  heart  sounds  in,  461, 

474 
blood-pressure  in,  30 
differential  diagnosis  of,  474 
effect  of  atropine  in,  472 
effect  of  iodides  in,  476 
effect  of  posture  on,  476 
etiological  factors,  472 
experimental,  465 
lesions  of  auriculoventricular 

bundle  in,  470 
occasional      confusion      with 
paroxysmal       tachycardia, 
475 
oesophageal  tracings  in,  474 
prognosis  in,  475 
relation  of  heart-block  to,  467 
stoppage  of  ventricles  in,  468 
stoppage  of  ventricles  in  tor- 
toise, 462 
syncopal  bradycardia,  460 
treatment  of,  476 
X-ray  examination  in,  474 
Adams-Stokes     syndrome     (Adams-Stokes 
disease),  460 
from  extrasystoles  alone,  471 
without  lesion  of  auriculoven- 
tricular bundle,  471 


Adenoids  as  cause  of  Basedow's  disease,  585 
asthma  due  to,  608 
cardiac  disturbances  due  to,  608 
Adherent  pericardium,  500 

absence  of  symptoms  from  intra- 

pericardial  adhesions,  500 
anginal  attacks  in,  291 
ascites  and  hydrothorax  in,  503 
ascites  in,  503 
Broadbent's    sign    (retraction    of 

ribs)  in,  504 
cardiac  dulness  in,  504 
cardiolysis  for,  510 
diastolic  shock  in,  505 
effect  on  circulation,  501 
fixation  of  lung  borders  in,  505 
hallucinations  in,  503 
hydrothorax  in,  503 
indications  for  cardiolysis,  510 
paradoxical   respiratory   ratio   in, 

504 
physical  signs  of,  504 
polyserositis  in,  509 
pseudocirrhosis  of  liver  in,  509 
pulse  in,  504 

pulsus  paradoxus  in,  504,  506 
reduplication  of  first  heart  sound 

in,  506 
Riegel's  pulse  in,  506 
sites  of  adhesions,  501 
sounds  over  stomach  in,  506 
third  heart  sound  and  shock  in, 

505 
treatment  of,  509 
X-ray  shadows  in,  507 
Adhesions,    pleural,    simulating    adherent 

pericardium,  505 
Adrenalin,  186 

production  of  aneurism  with,  525 
test  for  hyperthyroidism,  578 
Adrenals,  hypersecretion  in  arteriosclerosis, 

258 
Air  in  pericardial  cavity  (pneumopericar- 
dium), 494 
Air-swallowing,  604 

in  angina  pectoris,  296 
treatment  of,  605 
Albuminous  expectoration,  test  for,  150 
Albuminuria,  156 
Alcohol  as  cause  of  arteriosclerosis,  255 


616 


616 


INDEX. 


Alcohol,  cardiac  weakness  from,  611 

in  cardiac  disease,  168 
Allorrhythmias,  61 

classification  of,  62 
neurogenic,  62 
reflex,  63 

from  nose,  63 

from  stimulation  of  gastric  walls, 
63 
Amyl  nitrite,  action  of,  in  man,  187 
Anacrotic  pulse,  47 
Anaemia  in  cardiac  overstrain,  124 

in  endocarditis,  317 
Anatomical  terms,  synonymous,  xxiii 
Aneurism,  521 

age  of  occurrence,  523 

angina  pectoris  in,  291 

blood-pressure  in,  534 

brassy  cough  in,  530 

characteristics  at  various  sites,  537 

classification  of,  521 

delay  of  pulse  wave  in,  534 

development  of,  527 

diagnosis  of,  546 

differentiation  from   tortuous   arteries, 

546 
dilatation  of  pupils  in,  533 
dissecting,  547 

pathology  and  pathogenesis,  547 
symptoms  and  signs,  548 
dulness  over,  532 
dysphagia  in,  531 
electrolysis  in  (Moore-Corradi  method), 

552 
embolic,  526 
erosion  from,  527 
etiology,  522,  526 
experimental,  525 
frequency  of,  in  women,  523 
inequality  of  pulse  in,  534 
ligature  of,  method  of  Antyllus,  554 
method  of  Brasdor,  555 
method  of  Hunter,  554 
low  diet  (Tufnell's)  in,  551 
mesarteritis  in,  525 
multiple,  523 
murmur  in,  531 
mycotic,  526 
of  abdominal  aorta,  550 
pain  in,  550 
paralysis  in,  551 
rupture  of,  551 
tumor  in,  550 
of  the  heart,  234 
of  the  pulmonary  artery,  549 

signs  of,  549 
pain  in,  531 
pulsations  in,  532,  533 
role  of  syphilis  in,  522 
rupture  of,  527,  529 


Aneurism,  shock  in,  531 
sites  of,  522 

spontaneous  clotting  in,  529 
suffocation  in,  530,  531 
symptoms  of,  530 
tracheal  percussion  shock  in,  533 
tracheal  tug  in,  533 
treatment  by  compression,  554 

by  obliteration  of  sac  (Matas),  556 
by  occlusion  with  metal  bands,  555 
use  of  calcium  chloride  in,  552 
use  of  gelatin  in,  552 
use  of  potassium  iodide  for,  552 
venesection  in,  551 
wiring  of  (Moore's),  552 
X-ray  examination  in,  536 
Angeioneuroses,  274 

treatment  of,  278 
Angina  pectoris,  284 

and  palpitation,  286 
diagnosis  of,  294 
due  to  coronary  sclerosis,  288 
from  tobacco,  293,  610 
Heberden's  description  of,  284 
hysterical,  292 
importance  of  diet  in,  296 
in  acute  dilatation,  290 
in  aneurism,  291,  531 
in  children,  291 
in  hyperthyroidism,  293 
in  valvular  diseases,  290 
referred  pains  in,  287 
sudden  death  in,  288 
symptoms  of,  284 
theobromine  in  treatment  of,  185 
treatment  of,  185,  295 
varieties  of,  288,  292 
vasomotor,  291 
Anginal  pain,  theories  as  to  causation  of,  289 
Antagonistic  muscles,  contraction  of,   142, 

194 
Aorta,  dextroversion  (Rechtslage)  of,  433 
hypoplasia  of,  455 
stenosis  of  isthmus,  453 

adult  type,  454 
signs  of,  455 
treatment  of,  455 
type  of  new-born,  453 
Aortse,  primitive,  422 
Aortic  area,  102 

Aortic  disease  in  pregnancy,  419 
Aortic  facies,  367 
Aortic  insufficiency,  360 

amount  of  blood  regurgitating,  363 
and  mitral  stenosis,  differentiation 

between,  353 
asthma  from  lesion  of  nasal  septum 

in,  609 
blood-pressure  in,  29,  365,  372 
cardiac  outline  in,  368 


INDEX. 


617 


Aortic    insufficiency,  Cheyne-Stokes   respi- 
ration in,  366 

diagnosis  of,  376 

diastolic  murmur  in,  369 

double  murmur  (Duroziez's)  over 
the  arteries  in,  370 

Flint's  presystolic  rumble,  371 

functional,  360,  362 

hallucinations  in,  366 

historical,  360 

mitral  insufficiency  in,  377 

organic,  360 

pathological  physiology  of,  362 

precordial  pain  in,  366 

presystolic  thrill  in,  367 

prognosis,  376 

propagation  of  murmurs  in,  370 

pulmonary  circulation  in,  365 

pulse-rate  in,  365,  374 

relation  of  collapsing  pulse  to 
blood-pressure,  regurgitation, 
and  resistance,  373 

rupture  of  valves,  361 

sclerosis  of  aortic  valves,  361 

treatment,  376 

of  anginal  attacks  in,  379 

use  of  digitalis  and  strophanthus, 
377 

venesection  in,  378 

X-ray  shadow  in,  368 
Aortic  sclerosis,  263 
Aortic  stenosis,  381 

anacrotic  pulse  in,  386 

arrhythmia  in,  383 

atheromatous,  381 

blood-pressure  in,  387 

cardiac  outline  in,  384 

congenital,  452 

endocarditic,  381 

etiology  of,  382 

extrasystoles  in,  387 

failing  compensation  in,  383 

intraventricular  pressure  in,  383 

occurrence  of,  382 

pathological  anatomy,  381 

pulsus  tardus  in,  382,  385 

symptoms  of,  383 

thrill  and  murmur  in,  384 

treatment  of,  388 

with  aortic  insufficiency,  382 
Aortitis,  263 

acute,  254 
Apex  beat,  mechanics  of,  89 

method  of  recording,  89 

"mixed  type,"  91 

time  of,  89 
Apex  in  n^itral  insufficiency,  329 
Apnoea,  derivation  of,  in  cardiac  and  pul- 
monary diseases,  150 
Apoplexy,  blood-pressure  in,  29 


Arches,  visceral  (branchial),  423 
Arrhythmia,  61 

absolute,  75 

effect  of,  on  circulation,  77 

from  emotional  excitement,  612 

from  lesions  of  nasal  septum,  608 

in  increased  intracranial  tension,  64 

in  myocarditis,  238 

in  tricuspid  insufficiency,  402 

of  psychic  origin,  64 

permanent,  electrocardiogram  in,  77 

respiratory,  64 

vicious  circle  of,  78 

youthful  type,  64 
Arterial  tension,  18 

Arteries,   changes   in,   in  congenital   heart 
disease,  434 

normal  changes  in,  249 

sounds  in,  117 

strength  of  walls  of,  523 

tortuous,  resembling  aneurism,  546 
Arterionecrosis,  experimental,  from  adrena- 
lin, 257 
from  tobacco,  256 
from  toxins,  256 
in  animals,  256 
Arteriosclerosis,  249 

blood-pressure  in,  28,  261 

diet  in,  264,  265 

etiology  of,  254 

following  infectious  diseases,  255 

in  children,  258 

in  hypothyroidism,  575 

intermittent  claudication  from,  259 

nervous  symptoms  from,  259 

nitrites  in,  266 

of  abdominal  aorta,  260 

of  abdominal  vessels,  258 

of  retinal  vessels,  260 

potassium  iodide  in,  266 

pulse  in,  261 

role  of  salt  in,  258 

second  heart  sound  in,  263 

theories  of,  249,  257 

unity  of,  254 

use  of  warm  water  in,  265 

venesection  in,  266 

X-ray  examination,  260 
Arteriosclerotic  changes  in  vasa  vasorum,250 

lesions,  classification  of,  251 
distribution  of,  258 
Ascites,  155 

in  adherent  pericardium,  503 
Asphyxia,  effects  of,  27 
Aspiration  of  hydrothorax,  dangers  in,  156 
technic  of,  156  (see  also  Para- 
centesis) 
Astasia  abasia  in  Basedow's  disease,  584 
Asthma,  cardiac,  148 
Asthma  from  lesions  of  nasal  septum,  609 


618 


INDEX. 


Atrioventricular  bundle   (see  Auriculoven- 

tricular  bundle) 
Atrophy  of  the  heart,  211 
Atropine,  effect  of,  in  heart-block,  466 
effect  of,  on  changes  in  tonus,  13 
effect  of,  on  extrasystoles,  73 
test  in  heart-block,  472 
use  of,  in  pulmonary  oedema,  151 
Auricles,  mitral  stenosis  in  paralysis  of,  345 
Auricular  paralysis,  arrhythmia  in,  140 
cardiac  overstrain  in,  140 
venous  pulse  in,  57 
Auriculoventricular  bundle,  anatomy  of,  463 
clamping  of,  464 
lesions  of,  in  Adams-Stokes  disease, 

470 
physiology  of,  464 
Auscultation,  98 

in  suprasternal  notch,  102 
through  the  stomach  tube,  104 
Azygos  vein,  role  in  hydro  thorax,   155 


Bacterial  vaccines  in  treatment  of  endo- 
carditis, 311 
Basedow's  disease,  574,  576 
acute,  587 

anginal  attacks  in,  586 
arrhythmia  in,  583 
astasia  abasia  in,  584 
blood  count  in,  581 
blood-pressure  in,  30,  583 
calcium  salts  in,  588 
diagnosis  of,  585 

in  "formes  frustes,"  586 
etiological  factors,  579 
eye  signs,  583 

Dalrymple,  583 

Mobius,  583 

V.  Graefe,  583 

V.  Stellwag,  583 
force  of  heart  in,  582 
galvanization  of  cervical  sympa- 
thetic, 588 
Joffroy's  sign  of,  581 
loss  of  weight  in,  584 
metabolism,  581 
mortality  in,  587, 
psychic  symptoms,  582 
psychotherapy  in,  588 
relation  to  hysteria,  579 
secondary  to  adenoids,  585 
specific  sera  in,  588 
spontaneous  recovery  in,  587 
sympathectomy  for  (Jonnesco), 

590 
symptoms  and  signs  of,  581 
tachycardia  in,  582 
thyroidectomy  for,  589 

indications  for,  589 


Basedow's  disease,  thyroidectomy  for,   re- 
sults of,  589 
treatment  of,  587 
tremor  in,  584 

triad  and  tetrad  of  symptoms,  580 
wet  packs  in,  588 
X-ray  treatment  of,  588 
Baths,  Nauheim,  artificial,  201 
Nauheim,  natural,  201 
physiological  action  of,  200 
precautions  of,  200,  201 
Bathycardia,  603 
Beer  in  cardiac  disease,  168 
Belts,  effect  of,  in  producing  cardiac  over- 
strain, 134 
Bicycle  riding,  effect  of,  on  heart,  133 
Bigeminal  pulse,  72 

causes  of,  74 
Bigeminus,  69 
full,  69 
shortened,  69 
Bleedings  in  congenital  heart  disease,  437 
Blood  count  in  congenital  heart  disease,  441 
Blood  flow  through  muscles  during  exercise, 

129 
Blood,  viscosity  of,  38 
Blood-pressure,  18,  141 

apparatus,  Erlanger's  with  Hirsch- 
felder's  polygraph  attachment,  52 
apparatus,  forms  of,  23 
changes  in  exercises  of  speed,  130 
determination  of,  auscultatory 
method  for,  23 
of  maximal,  19 
of  minimal,  20 
Erlanger,  21 
Janeway,  20 
Masing,  20 
Mosso,  20 
Sahli,  20 
Strasburger,  20 
effect  of  digitalis  on,  175 
effect  of  exercises  of  strain  on,  132 
end  pressure,  18 
in  aortic  insufficiency,  365 
in  Basedow's  disease,  583 
in  different  parts  of  the  vascular 

system.  23 
in  normal  individuals,  23 
in  paroxysmal  tachycardia,  566 
in  various  diseases,  28 
lateral  pressure,  18 
maximal,  19 
minimal,  19 
physiological    factors    influencing, 

25 
variations  in,  under  physiological 
conditions,  26 
Blowing  diastolic  murmur  in  mitral  stenosis, 
351 


INDEX. 


619 


Blue  babies,  437 
Bradycardia,  48 

in  Adams-Stokes  disease,  460 
Brain  tumors,  blood-pressure  in,  29 
Brandy  in  cardiac  disease,  168 
Brauer  chamber  in  operations  on  heart,  517 
Breath-holding  test,  150 
Breathing,  Cheyne-Stokes,  152 
Broken  compensation  as  indication  for  in- 
ducing labor,  417 

blood-pressure  in,  30 

functional  valvular  insufficiencies 
in,  139 

pseudo-elephantiasis  in,  154 

pulmonary,  139 

systemic,  138 

venous  pressure  in,  141 
Broken  pulmonary  compensation  in  mitral 

insufficiency,  327 
Bronchitis  in  mitral  insufficiency,  334,  337 


Cachexia,  blood-pressure  in,  32 
Caffeine,  184 

in  cup  of  coffee,  169 
Calcification  in  arteriosclerosis,  252 

pathogenesis  of,  252 
Calcium  chloride  for  aneurism,  552 
Calcium  salts  as  cardiac  tonics,  184 

effect  of,  on  cardiac  contraction,  2 
in  Basedow's  disease,  588 
Calomel,  170 
Camphor,  183 
Canalis  auricularis,  423 
Capillaries,  changes  in,  in  congenital  heart 
"disease,  434 
determination  of  the  pressure  in,  33 
malformation  of,   in  congenital  heart 
disease,  435 
Capillary  pulse  in  aortic  insufficiency,  367 
Carbon  dioxide,  effects  of,  27 
Cardiac  and  adrenal  hypertrophy,  208 
Cardiac  area,  diameter  of,  95 
Cardiac  asthma,  148 

from  coronary  sclerosis,  283 
from  nasal  disease,  149 
Cardiac  cicatrices,  234 
Cardiac    dilatation,   mountain    sickness   as 
cause  of,  127 
recovery  from,  127 
transitory,  127 

fright  as  cause  of,  127 
Cardiac  disease,  symptoms  of,  147 
Cardiac  diseases,  acute,  blood-pressure  in,  32 
Cardiac  disturbances  due  to  myoma,  607 
due  to  sexual  disorders,  606 
in  females,  606 
in  males,  606 
from  lesions  of  nasal  septum,  608 
from  masturbation,  606 


Cardiac  disturbances,  reflex,  604 

air-swallowing  in,  604 
associated  symptoms,  604 
gastro-intestinal,  604 
relation  to  menstrual  flow,  607 
sexual,  treatment  of,  608 
Cardiac  dulness  area  in  children,  96 

relative,  93 
Cardiac  dyspnoea,  morphine  and  strychnine 

in,  149 
Cardiac  efficiency,  functional  tests  of,  141 
Cardiac  facies,  159 

Cardiac  failure  with  a  small  heart,  141 
Cardiac  flatness,  96 

absence  of,  96 

fixation   of  area  of,   in   adherent 

pericardium,  505 
pear-shaped,   in  pericarditis  with 

effusion,  490 
variations  in,  96 
Cardiac  impulse,  89 
course  of,  4 
mechanics  of,  89 
movements  in,  90 
origin  of,  4 

protodiastolic  wavelet  on,  90 
Cardiac  muscle,  tonicity  of,  11 
Cardiac  nerves,  action  of,  13 

effect  of  exercise  on,  14 
excision  of,  14 
tonic  action  of,  13 
Cardiac  neurasthenia,  593 
Cardiac  neuroses,  593 

arrhythmia  in,  593 
classification  of,  595 
sexual,  606 
symptoms  of,  593 
venous  pressure,  593 
Cardiac  overstrain,  anaemia  in,  124 

as  cause  of  Adams-Stokes  disease, 

473 
auricular  paralysis  and  arrhythmia 

in,  140 
cases  of,  121 
chlorosis  in,  124 
diagnosis  of,  128 
dilatation  of  heart  in,  125 
extrasystoles  in,  126 
mountain  climbing  as  6ause  of,  124 
precordial  pain  in,  125 
primary,  121 

etiology  of,  124 
sexual  excess  as  cause  of,  124 
tight  belts  as  cause  of,  124 
Cardiac  shadow  as  an  index  of  cardiac  vol- 
ume, 13 
Cardiac  tonicity,  effect  of,  on  regurgitation, 

363 
Cardiac   tonus  in  functional   insufficiency, 
324 


620 


INDEX. 


Cardiac  volume,  cardiac  shadow  as  an  index 
of,  13 

Cardiohepatic  angle  (Ebstein's)  in  pericar- 
dial effusion,  489 

Cardiolysis  for  relief  of  adherent  pericar- 
dium, 510 

Cardiometer,  9 

Cardiopathia  thyreopriva  (hypothyroidism), 
575 

Cardioptosis,  596 

Cardiosclerosis,  235 

Cardiosphygmograph,  52 

Cerebral  thrombosis,  blood-pressure  in,  29 

Chest,  flat,  in  congenital  heart  disease,  440 

Cheyne-Stokes  breathing,  152 
from  acapnia,  152 
treatment  of,  153 
types  of,  152 

Chlorosis  in  cardiac  overstrain,  124 

Choc  en  dome,  367 

Cholera,  blood-pressure  in,  32 

Chronic  hypertrophy  of  the  heart,  blood- 
pressure  in,  29 

Circulation  in  fcEtus,  mechanics  of,  427 

Claudication,  intermittent,  273 

Clubbed  fingers  in  congenital  heart  disease, 
439 

Coffee,  effect  of,  611 
prohibition  of,  169 

Coitus,  avoidance  of,  in  cardiac  disease,  419 

Cold  applications  over  the  heart,  164 

Collapse,  blood-pressure  in,  32 
hypotension  in,  32 

Collapsing  pulse,  47 

Compensation,  broken,  hydraemia  in,  39 
broken  pulmonic,  138 
broken  systemic,  138 
symptoms  of  broken,  138 

Concato's  arch  in  pericarditis  with  effusion, 
490 

Concretio  pericardii  cum  corde,  500 

Connective-tissue     proliferation,     interfas- 
cicular, 235 

Constipation,  effect  on  heart,  605 

Constricting  the   femoral   arteries,    rise   of 
blood-pressure  on,  142 

Constriction,  effect  of,  in  producing  cardiac 
overstrain,  134 

Contractility,  diminished,  in  pulsus  alter- 
nans,  67 

Contractions  of  heart,  maximal,  4 

Conus  arteriosus,  dilated,  in  mitral  stenosis, 
;347 

Convulsions  in  congenital  heart  disease,  437 

Coordination  of  the  cardiac  chambers,  7 

Cor  biatriatum  triloculare,  434 

Coronary  arteries,  distribution  of,  280 
ligation  of,  280 
sclerosis  of,  281 
vasomotor  nerves  in,  281 


Coronary  circulation,  physiology  of,  280 
Coronary  sclerosis  in  patients  with  paroxys- 
mal tachycardia,  283,  562 
symptoms  of,  283 
Corrigan's  pulse,  47 
"Corset  heart,"  600 

Corsets,  effect  of,  in  producing  cardiac  over- 
strain, 134 
Cough,  153 

(brassy,  stenotic,  paretic)  in  aneurism, 
530 
Cyanosis,  blood-pressure  in,  30 

in  congenital  heart  disease,  theories  of, 

438 
in  pulmonary  stenosis,  437 
in  tricuspid  stenosis,  408 


Dalrymple's  sign  in  Basedow's  disease,  583 
Death  from  labor,  cause  and  frequency  of, 

414 
Degeneration,  calcareous,  224 
hyaline,  224 
parenchymatous,  224 
waxy,  224 
Delusions,  160 

from  digitalis  poisoning,  160 
typical,  161 
Determination  of  the  blood-pressures,  aus- 
cultatory method  for,  23 
Dextrocardia     (dexiocardia),     relation     to 

transpositions  in  embryo,  456 
Diaphragm,  high,  603 

high,  in  fat  persons,  603 
Diarrhoea,  blood -pressure  in,  32 
Diastasis  and  diastole,  9 
Diastole  and  diastasis,  9 

position  of  the  valves  in,  10 
Diastolic     closure     of     auriculoventricular 

valves,  10,  56 
Dicrotic  notch,  time  of,  in  cardiac  cycle,  55 
pulse,  47 
wave,  45 

of  pulse,  45 
Diet,  167 

Carell's,  168 

effect  of,  on  viscosity,  39 
in  cardiac  disease,  167 
lacto-vegetarian,  167 
limited  milk,  168 
restricted  hquids  (Carell),  168 
restriction  of  salts,  168 
Digalen,  176 

Digestive  disturbances,  159 
Digitalis,  172,  176 
action  of,  174 

on  coronarj'  arteries,  175 
stage  of  incoordination,  174 
stage  of  irregularity,  174 
therapeutic  stage,  174 


INDEX. 


621 


Digitalis,    administration    in    fresh    mitral 
endocarditis,  337 
and  nitrites,  179 

and    strophanthus    in    aortic    insuffi- 
ciency, 377 
arrhythmia  and  heart-block  caused  by, 

179 
drugs  of  series,  172,  173 
effect  of,  on  normal  heart,  174 
effect  of,  on  the  blood-pressure,  175 
effect  of,  on  tonicity,  176 
flavoring  of,  178 
hallucinations  from,  180 
in  second  stage  of  mitral  insufficiency, 

338 
in  weakened  hearts,  179 
methods  of  administration,  178 
period  of  administration,  178 
poisoning,  delusions  from,  160 
preparations  of,  173 

choice  of,  176 
rectal  administration  of,  178 
standardization  of,  173 
Digi  toxin,  176 

Dilatation  of  the  heart,  acute,  angina  pec- 
toris in,  290 
acute,  pain  due  to,  289 
from  constriction,  134 
in  cardiac  overstrain,  125 
in  myocarditis,  227 
physiological  factors  bringing 

about,  135 
transitory,  127 
Diphtheria  as  cause  of  endocarditis,  303 

blood-pressure  in,  31 
Diplococcus  rheumaticus,  301 
Displacement  of  the  heart,  595 
Drugs,  mode  of  action  on  circulation,  172 
Duct  of  Cuvier,  422 
Ductus  arteriosus  (Botalli),  closure  of,  449 

factors  causing  persistence  of, 

449 
open,  434 
patent,  448 

diagnosis  of,  452 
murmur  in,  450 
pathogenesis  of,  448 
pulsus  paradoxus  in,  451 
respiratory      interchange 

in,  452 
signs  of,  450 
symptoms  of,  450 
treatment  of,  452 
X-ray  shadow  in,  450 
role  in  foetus,  428 
Ductus  venosus,  atrophy  of,  429 
Duroziez's  double  murmur  over  the  arteries 

in  aortic  insufficiency,  370 
Dysentery,  blood-pressure  in,  32 
Dyspnoea,  147 


Dyspnoea  in  congenital  heart  disease,  437 
mechanical  changes  in  circulation,  147 


Ebstein's  cardiohepatic  angle  in  pericardial 

effusion,  489 
Ectopia  cordis,  429 
Effusion  in  pericarditis,  487 
Electricity  in  treatment  of  angina  pectoris, 

297 
Electrocardiogram,  60 
in  extrasystoles,  70 
in  hypertrophy  of  left  ventricle,  60 
in  hypertrophy  of  right  ventricle,  60 
Embolism  in  mitral  stenosis,  356 

pulmonary,  151 
Embryocardia,  104 

in  paroxysmal  tachycardia,  568 
Emotion,  arrhythmia  from,  612 
effect  of,  on  the  heart,  612 
Emptying  of  the  heart,  8 
Endarteritis,  251,  253 

Endocarditic  vegetations,  bacterial  origin, 
299 
development  of,  299 
Endocarditis,  299 
anaemia  in,  317 
cerebral  embohsm  in,  308 
cerebral  type,  308 
choked  disk  in,  308 
chronic,  300,  306 
chronic  infective,  309 
complications  of,  315 
differential  diagnosis  of,  309 
digitalis  in,  316 
due  to  pyogenic  cocci,  302 
effect  on  circulation,  304 
from  miscellaneous  infections,  303 
gonorrhoeal,  303 
involvement  of  valves,  312 
jaundice  in,  307 
malignant,  305,  306 
complications,  306 

brain  symptoms,  306 
embolic  aneurisms,  306 
enlarged  spleen,  306 
haematuria,  306 
heart  failure,  306 
petechise,  306 
retinal  hemorrhages,  306 
frequency  of,  306 
valves  involved  in,  306 
microbes  producing,  301 
mural,  300 

palliative  treatment  of  tonsils  in,  318 
pathological  physiology  of,  304 
pathology  of,  300 
pneumococcic,  303 
prophylaxis,  317 
reinfection,  315 


622 


INDEX. 


Endocarditis,  retinal  hemorrhages,  308 

rheumatic,  301,  311 

septicaemic,  307 

simple  acute,  305,  311 

compensation  in,  315 
course  of,  314 
pathology  of,  313 
signs,  314 
symptoms  of,  313 

statistics  of,  311 

treatment  of,  317 

typhoidal  type,  308 

ulcerative,  300 
Endocardium,  atheroma  of,  304 

pockets  of,  in  aortic  insufficiency,  433 
EndotheUal  cells  in  sputum,  153 
Endurance,  exercises  of,  131 
Energy,  waste  of,  in  fatigue,  131 
Enteroptosis  (see  Splanchnoptosis) 
Epilepsy,  blood-pressure  in,  29 
Ergotism,  resemblance  to  RajTiaud's  dis- 
ease, 275 
Erosion  of  bone  by  aneurism,  527 
Erythromelalgia,  274 
Erythromeha,  277 
Exercise,  choice  of,  198 

effect  of,  on  blood-pressure,  26 

systems  of,  in  therapeutics,  193 

test  of  cardiac  function,  142 
Exercises,  effect  of,  on  size  of  heart,  133 

of  endurance,  131 

circulation  in,  131 
mechanics  of,  129 

of  speed,  mechanics  of,  129 

of  strain,  132 

effect  on  blood-pressure,  132 
mechanics  of,  129 
Exophthalmic  goitre  (see  Basedow's  disease) 
Exophthalmos  from  stimulation  of  sjmapa- 

thetic,  583 
Extrasystoles,  68 

auricular,  69 

auriculo(atrio)ventricular,  73 

auriculoventricular,  lesions  in,  74 

diagnosis  of,  71 

effect  of  atropine  on,  73 

electrocardiogram  in,  70 

experimental  production  of,  71 

heart  sounds  in,  72 

in  cardiac  overstrain,  126 

in  myocarditis,  238 

ineffectual,  72 

palpitation  with,  71 

stimuli  causing,  70 

venous  pulse  in,  70 

ventricular,  69 


Face,  oedema  of,  154 
Facies,  aortic,  88 


Facies,  cardiac,  88,  159 

mitral,  88 
Fatigue,  effect  of,  on  energy  used  up,  131 
Fats,  diminished  absorption  of,  159 
Fatty  degeneration  of  the  heart,  219 
etiology,  221 
nature  of,  220 

pathological  anatomy  of,  219 
rupture  of  the  heart  in,  223 
strength  of  heart  with,  221 
symptoms  and  signs  of,  222 
Fatty  infiltration  of  the  heart,  214,  215 

ndture  of  the  fatty  deposit, 

215 
physical  signs  of,  217 
treatment  of,  217 
Fetal  heart  sounds,  graphic  record  of,  104 
Fevers,  acapnia  in,  31 
Filling  of  the  heart,  8 

of  the  ventricles,  9 
First  sound  at  aorta,  100 
cause  of,  99 
character  of,  99 
duration  of,  100 
in  suprasternal  notch,  100 
reduplicated,  104,  105 
Fluoroscope,  82 

diagnosis  by,  85 
Foetus,  circulation  in,  427 
Football  playing,  effect  of,  on  heart,  133 
Foramen  ovale,  development  of,  425 

effect  of  patency  on  circulation,  447 
open,  434 
patent,  446 

crossed  embolism  in,  448 
occurrence  and  pathogenesis, 

446 
paroxysmal  cyanosis  in,  448 
signs  of  patency,  448 
symptoms  of  patency,  447 
treatment  of,  448 
vicious  circle  in,  436 
Formative  stimulus  in  arteriosclerosis,  253 
Fragmentation  of  muscle  fibres,  225 
Friction  in  pericarditis,  484 

pleuropericardial,  484 
Functional  mitral  insuflficiencj',  322 
Functional  tests  of  cardiac  efficiency,  141 
of  cardiac  insufficiency,  valueof,  143 
relation  of,  to  mode  of  life,  143 


Gallop  rhythm,  presystolic,  105,  106 

protodiastolic,  105,  107 
Gastric  ferment  action,  604 
Gonococcus  as  cause  of  endocarditis,  303 
Graefe's  sign  in  Basedow's  disease,  583 
Graves's  disease  (see  Basedow's  disease) 
GjTnnastics,  193 

fundamental  principles  of,  193 


INDEX. 


623 


Hsemopericardium,  493 

from  cardiac  tumors,  246 
Haemoptysis  from  pulmonary  stasis,  151 

in  pulmonary  insufficiency,  392 
Hsemosiderin  in  Herzfehlerzellen,  153 
Hallucinations,  160 

in  adherent  pericardium,  503 
Headaches  in  congenital  heart  disease,  437 
Heart,  changes  in  position  of,  97 
changes  in  size  of,  97 
development  of,  early  stages,  421 
dilatation  of,  from  constriction,  134 
diminution  in  size  of,  in  exercise,  133 
disease  and  matrimony,  419 
congenital,  421 

blood  count  in,  441 
etiological  groupings,  430 
flat  chest  in,  440 
groups  of  lesions  in,  429 
syndrome  of,  430 
displacement  of,  595 

effect  on  circulation,  596 
endothelial  tube  in  embryo,  422 
high,  604 

effect  on  circulation,  604 
treatment  of,  604 
xiphisternal  line  with,  604 
insensibility  of,  286,  515 
lesions,  congenital,  classification  of,  429 
low,  596,  603 

signs  of,  603 
mobility  of,  in  cardioptosis,  596 
muscle,  properites  of,  1 

structure  of,  1 
muscular  tube  in  embryo,  422 
non-perforating  injuries  of,  518 
normal  mobility,  596 
nourishment  of,  281 
small,  in  cardiac  failure,  141 
sound,  first,  reduplication  of,  in  adhe- 
rent pericardium,  506 
second  aortic,   in  arteriosclerosis, 

263 
second,  in  mitral  insufficiency,  333 
third,  in  adherent  pericardium,  505 
sounds,  accessory,  104 
causes  of,  99 
clinical  diagram  for,  99 
digital  imitation  of,  115 
graphic  record  of,  98 
reduplicated,  104,  105 
split,  105 
three-chambered,  434 
tumors  of,  245 
work  of,  26 
wounds  of,  513 

cause  of  death  from,  514 
experimental  surgery  of,  513 
hemorrhage  in,  517 
murmurs  in,  515 


Heart,  wounds  of,  operative  treatment  of,  515 
spontaneous  recovery  in,  513 
suture  of,  516 
symptoms  of,  515 
X-ray  examination  of,  515 
Heart-beat,  origin  of,  2 
Heart-block    (see   also    Adams-Stokes    dis- 
ease), 65,  460,  462 
auriculoventricular,  66 
complete,  66,  466 
effect  of  atropine  on,  466 
effect  of  vagus  on,  466 
from    cutting    interauricular   sep- 
tum, 461 
functional,  66 
in  infectious  diseases,  472 
in  tortoise,  462 
organic,  66 
'  partial,  66,  466 

effect  of  heart  rate  in,  466 
from  digitalis,  473 
relation    to     Adams-Stokes    syn- 
drome, 467 
role  of  vagus  in,  461 
sino-auricular,  67 
Hemorrhage,  blood-pressure  in,  32 
fall  of  blood-pressure  in,  32 
from  the  lungs,  151 
in  wounds  of  heart,  517 
intracranial,  blood-pressure  in,  29 
Heredity  in  arteriosclerosis,  256 
Herzfehlerzellen,  153 
Hiccough  in  pericarditis,  483 
High  diaphragm,  603 

heart,  604 
Hippocratic  fingers,  439 
His  bundle,  anatomy  of,  463 
Hoarseness  in  pericarditis,  483 
Hormone  action  in  cardiac  symptoms,  608 
Hydropericardium,  493 
Hydrotherapy,  200 

in  arteriosclerosis,  265 
Hydrothorax,  155 

in  adherent  pericardium,  503 
production  of,  155 
Hyperdicrotic  pulse,  47 
Hypertension   as   factor   in   production   of 
arteriosclerosis,  257 
diseases  with,  28 
Hyperthyroidism,  576 

acetonitrile  test  for,  578 
adrenalin  test  for,  578 
angina  pectoris  in,  293 
effect  on  heart  muscle,  578 
effect  on  nervous  system,  578 
vicious  circle  of,  579 
Hypertrophied  heart,  reserve  force  of,  210 
Hypertrophy,  203 
adrenaf,  208 
and  abdominal  arteriosclerosis,  208 


624 


INDEX. 


Hypertrophy  and  arteriosclerosis,  207 

cardiac,  208 

concentric,  205 

excentric,  205 

from  overdrinking,  207 

from  work,  205 

in  chronic  nephritis,  207 

of  the  auricles,  210 

of  the  heart  in  Basedow's  disease,  583 

of  the  left  ventricle,  209 

of  the  right  ventricle,  209 

pathological  anatomy  of,  203 

sites  of,  205 
Hypotension,    failure  of  vasomotor   centre 

in,  30 
Hypothyroidism,  effect  on  circulation,  575 
Hysterical  angina,  292 


Ice-bag  over  heart,  165 

contraindications  to,  165 
effect  on  pulse  rate,  165 
Increased  intracranial  pressure,  blood-pres- 
sure in,  29 
Infectious  diseases  as  causes  of  arteriosclero- 
sis, 255 
as  causes  of  Basedow's  disease,  579 
hypotension  in,  31 
Influenza  as  cause  of  Basedow's  disease,  580 

as  cause  of  endocarditis,  303 
Injuries  of  heart,  518 
Insufficiency,  mitral,  321 

of  valves  in  broken  compensation,  139 
Intermittent  claudication,  273 
Interstitial  pneumonia,  153 
Intervenous  area,  physiology  of,  7 
Interventricular  septum,  defects  in,  442 
patent,  442 

with  pulmonary  stenosis,  433, 
437 
Intravenous  injections  in  treatment  of  endo- 
carditis, 311 
Intraventricular  pressure,  18 
lodothyrin,  576 
Irregularity,  permanent,  76 
Irritability  in  cardiac  disease,  160 


Jaundice,  catarrhal,  in  broken  compensa- 
tion, 159 
in  endocarditis,  307 
Jellinik's  sign  of  Basedow's  disease,  579 
Joffroy's  sign  of  Basedow's  disease,  581 


Labor  (see  Pregnancy) 

and  pregnancy  in  persons  with  heart 
disease,  prognosis,  415 

cardiac  overstrain  during,  414 
Langendorff's  perfusion  apparatus,  3 


Laryngeal  paralysis  in  aneurism,  530 
Lead  poisoning,  blood-pressure  in,  29 
Left  auricle,  pressure  in  fetal  life,  429 
Liquids,   restriction  of,   in  arteriosclerosis, 

265 
Liver,  abdominal  pain  from  distended,  159 
presystolic  pulsation  in  tricuspid  steno- 
sis, 408 
pulsation  of,  in  tricuspid  insufficiency, 

402 
signs  simulating  cirrhosis  of,  in  adhe- 
rent pericardium,  509 
Low  heart,  603 
Lungs,  hemorrhage  from,  151 


Magnesium  sulphate,  170 
Marching,  effect  of,  on  heart,  133 
Masturbation,  effect  of,  on  heart,  606 
Matrimony  and  heart  disease,  419 
Meals,  effect  of,  on  blood-pressure,  26 
Measles,  blood-pressure  in,  31 
Mechanical  factors  in  the  production  of  mur- 
murs, 109 
Mechanogymnastics,  197 
Medial  changes  in  aneurism,  525 
Mediastinopericarditis,  500 
Meningitis,  blood-pressure  in,  29 
Menstruation,  relation  of,  to  cardiac  symp- 
toms, 607 
Mental  distraction,  163 

exertion,  effect  of,  on  blood-pressure,  27 
Mesarteritis,  251,  252 
Metabolism,  increase  from  thyroid  secretion, 

577 
Micrococcus  rheumaticus,  301 
Mid-diastolic  nunble  stenosis,  350 
Mill-wheel  murmur  in  pneumopericardiimi, 

494 
Mitral  area,  102 
Mitral  disease,  pulmonary  complications  of, 

327 
Mitral  facies  in  mitral  insufficiency,  329 
Mitral  insufficiency,  321 

and  tuberculosis,  336 
arrhythmia  in,  334 
blood -pressure  in,  333 
broken  compensation  in,  339 
broken    pulmonary   compensation 

in,  327 
broken  systemic  compensation  in, 

328 
cardiac  area  in,  330 
digitalis  in,  338 
earlv  administration  of  digitalis  in, 

.337 
functional,  322,  323,  324 
mechanics  of,  circulation,  324 
murmur  and  sounds  in,  331 
oesophageal  tracing  in,  58 


INDEX. 


625 


Mitral  insufficiency,  organic,  321 

outward  displacement  of  apex  in, 

329 
papillary,  322 
pathology  of,  321 
prognosis  in,  339 
propagation  of  murmur,  332 
pulmonary  stasis  in,  325,  336 
purgation  in,  338 
re-education  of  heart  muscle  in, 

337 
relative,  322 

second  heart  sound  in,  333 
second  stage  of,  327 
stages  of,  326 
stasis  in  left  auricle,  324 
statistics  of,  321 
systolic  murmur  in,  331 
third  stage  of,  328 
tonicity  of  the  heart  in,  328 
treatment  of  second  stage  of,  338 
with  mitral  stenosis,  349 
without  symptoms,  326 
X-ray  shadow  in,  330 
Mitral  stenosis,  341 

anaemia  in,  357 

and  aortic  insufficiency,  differen- 
tiation between,  353 
and  tricuspid  stenosis,  355 
blood-pressure  in,  32 
blowing  diastolic  murmur  in,  351 
cardiac  outline  in,  347 
complications,  355 
congenital  form,  342 
diagnosis,  352 
digital  and  phonetic  imitation  of 

the  heart  sounds  in,  349 
dilated  conus  arteriosus  in,  347 
disappearance    and    reappearance 

of  presystolic  rumble  in,  345 
effect  of  auricular  contraction  on 

filling  of  ventricles,  344 
embolism  in,  356 
endocarditic  form,  342 
etiology,  342 
historical,  341 
laryngeal  paresis  in,  345 
mid-diastolic  rumble  in,  3^0 
operations  on  mitral  A^alve,  357 
paralysis  of  auricles  in,  345 
pathological  physiology  of,  343 
pathology  of,  341 
presystolic  rumble  in,  347 

thrill  and  systolic  tap  in,  346 
prognosis,  357 
pulmonary  oedema  in,  356 
pulse  in,  352 
quality    and    production    of    the 

sounds,  348 
role  of  oedema  and  anaemia  in,  342 
40 


Mitral  stenosis,  sclerotic  form,  342 

snapping  first  sound  in,  348 
stages  of,  351 
symptoms  and  signs,  345 
third  heart  sound  in,  350 
thrombosis  in  left  auricle  in,  356 
treatment  of,  356,  357 
tuberculosis  in,  342 
volume  of  ventricles  in,  343 
with  mitral  insufficiency,  342,  349 
X-ray  shadow  in,  348 
Mitral  valve,  atheroma  of,  323 
hemorrhage  in,  323 
malformation  of,  458 
tests  for  sufficiency,  322 
demonstration  of  action  of,  10 
Mitralized  pulse,  334 
Mobility  of  heart,  98 
Mobius'  sign  in  Basedow's  disease,  583 
Monckeberg's  arteriosclerosis,  251 
Moore-Corradi  method,   reasons  for  failure 

of,  553 
Morbus  coeruleus,  436 
Morphine,  dangers  from,  in  myocarditis, 
243 
in  cardiac  dyspnoea,  149 
Movements,  resisted,  194 

Schott,  194 
Murmur  at  back  in  patent  ductus  Botalli, 
440 
diastolic,    in   pulmonary   insufficiency, 

393 
mitral,  differentiation  from  accidental 
and  tricuspid,  332 
digital  imitation  of,  331 
phonographic  tracing  of,  331 
propagation  of,  332 
Roger's  systolic  in  open  septum  ventric- 

ulorum,  444 
systolic,  in  aortic  stenosis,  384 
in  mitral  insufficiency,  331 
in  tricuspid  insufficiency,  400 
Murmurs,  109 

accidental,  111 

causation  of,  113 
differential  diagnosis  of,  112 
nature  of,  113 
time  of,  112 
cardiopulmonary.  111,  114 
character  of,  110 

differentiation    between    cardiopulmo- 
nary and  other  accidental  murmurs, 
115 
functional,  111 
ha;mic.  111,  113 
mechanical  factors  in  the  production 

of,  109 
phonetics  of,  109 
tabulation  of,  116 
Myocardial  changes,  distribution  of,  225 


626 


INDEX. 


Myocarditis,  224 

acute,  arrhythmia  in,  228 

alcoholic,  231 

and  nephritis,  240 

arrhythmia  in,  237,  238 

bronchitis  in,  238 

catalase  in,  240 

chronic,  234 

blood-pressure  in,  237 

.diagnosis  of,  232 

differential  diagnosis  in,  241 

dilatation  in,  227 

diphtheric,  230 

extrasystoles  in,  238 

hypersensibility  to  digitalis,  233 

influenzal,  230 

murmurs  in,  238 

pathological  physiology  of,  236 

rheumatic,  229 

signs  and  symptoms  of,  229 

strychnine  in,  234 

symptoms  and  signs  of,  238 

treatment  of,  232,  242 

weakness  of  heart  in,  228 
Myocardium,  affections  of,  224 

syphilis  of,  244 
Myoma  as  cause  of  cardiac  weakness,  607 


Nasal  disease,  cardiac  asthma  from,  149 
Nasal  septum,  arrhythmia  from  lesion  of, 
608 
asthma  from  lesion  of,  609 
Nauheim  treatment,  164 
Nephritis  and  myocarditis,  240 

blood-pressure  in,  28 
Nerve-fibres  producing  changes  in  tonus,  13 
Neurasthenia,  cardiac,  593 
Nitrites,  186 

action  of,  187 

and  digitalis,  179 

effect  of,  in  hypertension  of  intracranial 

origin,  30 
use  of,  in  angina  pectoris,  295 

in  aortic  insufficiency,  377 
in  arteriosclerosis,  266 
Nitroglycerin,  186,  188 

mode  of  administration,  188 
tolerance  to,  188 


Oarsmen,  longevity  of,  137 
Obesity,  diet  in,  218 

high  diaphragm  in,  216,  603 

of  the  heart,  214 

physical  signs  of,  217 

treatment  of,  217 

with  cardiac  atrophy  and  cardiosclero- 
sis, 216 

with  coronary  sclerosis,  216 


(Edema,  153 

effect  of  drugs  and  diet  on,  154 

fluid,  salt  content  of,  154 

lymphagogue  substance  in  the  blood  in, 
153 

of  face,  154 

of  heart  muscle,  138 

pulmonary,  150 

treatment  by  drainage,  155 

types  of,  153 
Oertel's  mountain  climbing,  198 
(Esophageal  auscultation,  104 
of  mitral  murmur,  332 

tracings,  58 

in  mitral  insufficiency,  58 
Orthodiagraph,  85 
Orthopercussion,  93 
Orthoplessimeter,  94 
Orthopncea,  148 

mechanical  changes  in  circulation,  148 
Outflow  during  systole,  9 


Pain  down  the  arms,  158 

on  swallowing  in  pericarditis,  483 
precordial,  158 

referred  from  cervical  ganglia,  158 
sensations,  paths  traversed  by,  286 
Palpation  of  heart,  92 
Palpitation,  157 

and  angina,  286 
cardiac  sensations  in,  157 
with  extrasystoles,  71 
Papillary  insufficiency,  323 
muscles,  fatiguing  of,  55 

in  propagation  of  mitral  murmur, 
332 
Paracentesis  abdominis,  155 
Paradoxical  respiration  in  enteroptosis,  599 
Pararrhythmias,  62,  75 
Paroxysmal  tachycardia,  78,  560 
associated  lesions,  562 
auricular  fibrillation  in,  564 
belching  in,  572 

cardiac  dulness  during  attacks,  568 
cerebral  ansemia  in,  568 
coronary  sclerosis  in,  562 
diagnosis  of,  570 

differentiation  from  simple  tachy- 
cardia, 570 
doubling  of  rate  in,  560 
drugs  in,  571 
dyspnoea  in,  567 
effect  on  circulation,  566 
embryocardia  in,  568 
fall  of  blood -pressure  in,  566 
from  ligature  of  coronary  arteries, 

565 
fulness  of  neck  in,  567 
in  coronary  sclerosis,  283 


INDEX. 


627 


Paroxysmal  tachycardia,  inactivity  of  car- 
diac nerves  in,  565 
inception  of  rhythm  by  auriculo- 

vfentricular  bundle,  564 
interpolated  extrasystoles,  563 
lesions  in  auriculoventrieular  bun- 
dle in,  563 
lesions  in  vagus  nucleus,  563 
occasional  confusion  with  Adams- 
Stokes  disease,  475 
precordial  pain  in,  567 
rise  of  venous  pressure  in,  566 
sino-auricular  block,  464 
stimulation  of  vagi  in,  571 
sudden  exercise  in,  571 
swallowing  in,  572 
symptoms  of,  567 
theories  as  to  origin,  563 
treatment  of,  571 
triciispid  insufficiency  in,  568 
types  of,  561 
venous  pulse  in,  561 
vorhiting  in,  572 
Parry's  disease  (see  Basedow's  disease) 
Passive  movements,  194 
Patent  foramen  ovale,  466 

pathogenesis  of,  466 
Percussion,  92 
errors  in,  94 
methods  of,  93 
Perfusion  of  excised  mammalian  heart,  3 
Periarteritis,  diffuse,  252 
Periarteritis  nodosa,  251 
Pericarditis,  480 

adhesive    (see  Adherent  pericardium), 

500,  504 
blood-pressure  in,  32,  485 
etiology  of,  480 
friction  at  back  in,  485 
friction  sound  in,  484 
hiccough  in,  483 
hoarseness  in,  483 
pain  on  swallowing  in,  483 
precordial  pain  in,  483 
purulent,  493 
simple  fibrinous,  483 

diagnosis  of,  485 
prognosis  in,  487 
treatment  of,  486 
signs  of,  483 
symptoms  of,  483 
tuberculous,  494 
fluid  in,  494 
with  effusion,  487 

amount  of  fluid,  487 
blood-pressure  in,  491 
drainage  in,  497 
Ebstein's  cardiohepatic  angle 

in,  489 
effect  on  circulation,  487 


Pericarditis  with  effusion,  enlargement  of 
liver  from,  490 
fulness  of  interspaces  in,  489 
irrigation  of    pericardium    in, 

498 
paracentesis  of,  495 
pericardiotomy  in,  497 
position  of  heart  in,  490 
Rotch's  sign  in,  489 
signs  at  back  in,  490 
signs  of,  489 
symptoms  of,  488 
treatment  of,  495 
X-ray  examination  of,  491 
Pericardiimi,  adherent,  291,  500 

development  of,  426 
Peripheral  resistance,  44 
Peritonitis,  blood-pressure  in,  31 
Petechise  in  endocarditis,  307 
Phosphorus  poisoning,  effect  of,  on  heart  in 

fatigue,  134 
Phthisis,  blood-pressure  in,  31 
Physiological  conditions,  variations  in  blood- 
pressure  under,  26 
Pigmentation  in  hyperthyroidism  (Jellinik's 

sign),  579 
Placenta,  vessels  to,  422 
Pleurisy,  blood-pressure  in,  32 
Pleuropericardial  friction,  484 
Pneumococci  as  causes  of  endocarditis,  303 
Pneumonia  as  cause  of  pericarditis,  480 
blood-pressure  in,  31 
interstitial,  153 
Pneumopericardium,  494 
Polycythsemia,  blood-pressure  in,  30 
Polygraph,  Mackenzie,  52 
Marey,  52 
Uskoff,  53 
Position,  changes  in,  97 

effect  of  change  of,  on  blood-pressure,  26 
Posture,  effect  of,  on  pulse-rate,  142 
Potassium  iodide,  189 

effect  of,  on  viscosity  of  blood,  39 
for  aneurisms,  552 
in  angina  pectoris,  295 
in  arteriosclerosis,  266 
mode  of  administration,  189 
supposed    effect    on    viscosity    of 
blood,  189 
salts,  effect  of,  on  cardiac  contraction,  2 
thiocyanate,  190 

therapeutic  use  of,  190 
Precordial  pain,  158 

in  cardiac  overstrain,  125 
in  pericarditis,  483 
Pregnancy  and  labor,  pulmonary  oedema  in, 
414 
aortic  disease  in,  419 
as  cause  of  Basedow's  disease,  579 
blood-pressure  in,  30 


628 


INDEX. 


Pregnancy,  broken  compensation  in,  416 
effect  on  pulse  and  blood  pressure,  413 
hypertrophy  during,  413 
termination  of,  418 

in  broken  compensation,  417 
treatment  of  heart  lesions  during,  416 
Presphygmic  period,  8 
Presystolic  gallop  rhythm,  resemblance  to 
mitral  stenosis,  353 
rumble,   disappearance  and  reappear- 
ance of,  in  mitral  stenosis,  ;345 
(FUnt's)  in  aortic  insufficiency,  371 
in  mitral  stenosis,  347 
in  tricuspid  stenosis,  409 
Pseudo-anginal  pain,  289 
Pseudo-aortic  insufficiency,  367 
Pseudocardiac  disturbances,  595 
Psychic  disturbances,  159 
Psychotherapy  in  Basedow's  disease,  588 
Puerperal  infection  as  cause  of  Basedow's 

disease,  580 
Pulmonary  area,  102 
Pulmonary  artery,  aneurism  of,  549 

blood-pressure  in,  before  birth,  33 
development  and  maldevelopment 

of,  432 
sclerosis  of,  264 
vasomotor  nerves  in,  34 
Pulmonary  circulation,  33 

action  of  drugs  on,  34 
Pulmonary  embolism,  151 
Pulmonary  hemorrhage,  151 
Pulmonary  insufficiency,  diagnosis  of,  394 
diastolic  murmur  in,  393 
etiological  factors,  391 
forms  of,  390 
functional,  390 
haemoptysis  in,  392 
pathological  physiology,  391 
prognosis  in,  394 
pulse  in,  393 
signs  of,  392 
symptoms  of,  392 
treatment  of,  394 
with  pulmonarj'  stenosis,  440 
Pulmonary  oedema,  150 

artificial  respiration  in,  150 
in  mitral  stenosis,  356 
in  pregnancy  and  labor,  414 
signs  of,  150 
treatment  of,  151 
Pulmonary  pressure,  34 

conditions  affecting,  34 
Pulmonary  stenosis  and  atresia,  causes  of, 
430 
due  to  endocarditis,  430 
due    to    maldevelopment    of 

branchial  arches,  431 
duration  of  life  in,  441 
statistics  of,  430,  441 


Pulmonary  stenosis   in  open  interventric- 
ular septum,  439 
pathological  physiology  of,  435 
with  patent  interventricular  sep- 
tum, 433,  437 
Pulsations,  inspection  of,  532 

over  chest,  92 
Pulse,  anacrotic,  in  aortic  stenosis,  386 
arterial,  41 

curve,  significance  of,  44 
dicrotic,  41 

discrepancies  in  examining,  43 
examination  of  the,  41 
form,  44 

in  aortic  insufficiency  (Corrigan,  water- 
hammer,  collapsing),  372 
qualities  of  the,  41 
rate,  46 

effect  of  ice-bag  on,  165 
effect  of  posture  on,  142 
relation  to  temperature,  46 
types  of,  47 

anacrotic,  47 
bisferiens,  47 
collapsing,  47 
dicrotic,  47 
hyperdicrotic,  47 
normal,  47 
tardus,  47 
venous,  49 

wave,  inequality  and  delay  of,  in  aneu- 
risms, 534 
Pulse-pressure,  19 
Pulsus  alternans,    contractilitv    diminished 

in,  67 
Pulsus  tardus  in  aortic  stenosis,  382,  385 
Pupils,  inequality  of,  in  aneurism,  533 
Purgation,  169 

in  broken  compensation,  169 
rise  of  venous  pressure  during,  170 
Purgatives,  170 


Quiet  in  treatment,  163 


Radiographs,  technique  of,  86 

Raynaud's  disease,  274 

pathology  of,  275 

Rectal  administration  of  digitalis,  178 

RedupUcated  heart  sounds,  104 

Re-education  of  heart  muscle  in  mitral  in- 
sufficiency, 337 

Referred  pains  in  angina  pectoris,  287 

Reflex  cardiac  disturbances,  604 

air-swallowing  in,  604 
associated  symptoms,  604 
gastro-intestinal,  604 

Relative  insufficiency,  323 

Renal  complications  of  cardiac  diseases,  156 


INDEX. 


629 


Residual  blood,  12 

Respiration,  method  of  recording,  52 

paradoxical  type,  599 
Respiratory  ratio,  150 

in  adherent  pericardium,  504 
Rest  in  bed,  164 
Retina,  arteriosclerosis  of,  260 

dilatation  of  veins  of,  in  tricuspid  insuf- 
ficiency, 400 
Retinal  changes  in  congenital  heart  disease, 

438 
Rheumatic  fever  as  cause  of  pericarditis,  480 

foci  of  myocarditis  in,  226 
Rheumatism,  blood-pressure  in,  31 

cocci  causing,  301 
Riess'  sign  of  adherent  pericardium,  506 
Right  ventricle,  tonicity  of,  34 

work  of  the,  33 
Rise  of  blood-pressure  on  constricting  the 

femoral  arteries,  142 
Rotch's  sign  of  pericardial  effusion,  489 
Rupture  of  aneurism,  527 


"Safety-valve"  action  of  tricuspid  valve, 

397 
Salt,  restriction  of,  168 
Salts,  role  of,  in  origin  of  heart  beat,  2 
Sauerbnich  chamber  in  operations  on  heart, 

517 
Scarlatina  as  cause  of  endocarditis,  303 
blood-pressure  in,  31 
pericarditis  from,  481 
Schott  movements,  194 

effect  of,  in  reducing  cardiac  dila- 
tation, 197 
precautions  in,  195 
Second  sound,  100 
Second  wind,  130 

Sensory  stimulation,   effect   of,   on  blood- 
pressure,  27 
Septum  auriculorum,  424 
Septum  interpositum,  425 
Septum  ventriculorum,  424,  442 

patent,  effect  on  circulation,  443 
prognosis  in,  445 
signs  of,  443 
symptoms  of,  443 
systolic  murmur  in,  444 
trauma  as  cause  of,  442 
treatment  of,  445 
tuberculosis  in,  442 
Sexual  cardiac  disorders,  606,  608 
Sexual  excess  as  cause  of  Basedow's  disease, 

580 
Shock,  acapnia  in,  31 

blood-pressure  in,  31 
diastolic,  over  aneurism,  546 
Sino-auricular  block  from  cooling  sinus,  5 
in  mammals,  7 


Sino-auricular  block  in  paroxysmal  tachy- 
cardia, 564 
Sinus  as  "  paee-maker  "  of  the  heart,  4 
Sinus  region  in  mammals,  anatomy  of,  5 
Sinus  reuniens,  424 
Sinus,  role  of,  in  mammals,  6 
Sinus  wave  on  venous  pulse,  56 
Situs  transversus,  456 

Skull,  fracture  of  the,  blood-pressure  in,  29 
Sleep,  effect  of,  on  blood-pressure,  27 

importance  of,  163 
Smallpox  as  cause  of  endocarditis,  303 
Smoke,  tobacco,  composition  of,  609 
Smoking,  effect  of,  on  circulation,  610 

precordial  pain  from,  610 
Snapping  first  sound  in  aortic  insufficiency, 
371 
in  mitral  stenosis,  348 
Sounds,  alteration  of,  by  pressure,  101 

in  arteries,  117 

over  veins,  118 
Southey's  tubes,  155 
Spa  treatment,  164 
Sphygmobolometer,  Sahli,  23 
Sphygmogram,  the  absolute,  43 
Sphygmograph,  clinical,  41 

Dudgeon,  42 

V.  Jaquet,  42 

Marey,  42 

Roy  and  Adami,  42 
Sphygmography,  errors  in,  42 
Sphygmomanometer,  v.  Basch,  19 

Erlanger,  21 

Gibson,  23 

Hill  and  Barnard,  20 

Marey,  19 

Potain,  20 

v.  Recklinghausen,  19 

Riva-Rocci,  20 
Sphygmoscope,  Pal,  22 
Sphygmotonometer,  v.  Recklinghausen,  22 
Splanchnoptosis,  598 

abdominal  binder  in,  600 

air-cushion  for,  601 

blood-pressure  in,  599 

corset  in  producing,  600 

effect  on  circulation,  599 

effect  of,  on  respiration,  598 

level  of  diaphragm,  598 

overfeeding  in,  601 

pulsus  paradoxus  in,  600 

syncope  from,  599 

tracheal  tug  in,  599 

treatment  of,  600 
Sputum,  prune-juice,  151 
Stair  climbing,  beneficial  effects  of  graded 

pauses,  198 
Stasis,    effect    of,    on    producing   cardiac 

oedema,  138 
Stellwag's  sign  in  Basedow's  disease,  583 


630 


INDEX. 


Stenosis  of  isthmus  of  aorta,  453 
Sterilization  of  patients  with  broken  com- 
pensation, 419 
Stethoscope,  binaural,  essentials  of,  101 

monaural,  100 
Stomach,  sounds  over,  in  adherent  pericar- 
dium (Riess),  506 
Stoppage  ot  ventricles,  465 

in  Adams-Stokes  disease,  468 
Strain,  effect  of,  on  the  heart,  136 

exercises  of,  132 
Strophanthus,  173 
Strychnine,  181 

and  digitalis,  316 
clinical  effects,  181 
effect  on  blood-pressure,  182 
effect  on  cardiac  tonicity,  181 
in  cardiac  dyspnoea,  149 
indications  for,  183 
pharmacological  action  of,  181 
preparations  of,  181 
Sudden  death  in  angina  pectoris,  288 
Suture  of  wounds  in  heart,  516 
Swimming,  effect  of,  on  heart,  133 
Sympathectomy  in  Basedow's  disease,  590 
Sympathetic  nerves,  relation  to  exophthal- 
mos, 583 
stimulation  by  thyroid  secretion, 
577 
Symptoms  of  adherent  pericardium,  503 

of  cardiac  disease,  147 
Syncope  in  paroxysmal  tachycardia,  568 
Synechiae  pericardii,  500 
Syphilis  as  cause  of  arteriosclerosis,  155 
as  cause  of  endocarditis,  304 
in  etiology  of  aneurism,  522,  526 
of  the  myocardium,  244 

with  precordial  pain,  244 
Systolic   murmur   in    mitral    insufficiency, 
331 
retraction    along    left  cardiac   border, 

329 
retractions  over  heart,  91 


Tabagism,  610 

Tachycardia,  paroxysmal,  560 

Tea,  effect  of,  611 

prohibition  of,  169 
Tests,  functional,  of  cardiac  efficiency,  141 
Theobromine,  185 

in  angina  pectoris,  185,  296 
Theocin,  185 

Theophylline  in  angina  pectoris,  296 
Theories  of  heart -beat,  3 

myogenic,  3 

neurogenic,  3 
Third  heart  sound,  frequency  of,  in  normal 
individuals.  109 

in  aortic  insufficiency,  371 


Third  heart  sound  in  mitral  stenosis,  350 
mechanism  producing,  107 
Thread  galvanometer,  60 
Threshold  percussion,  93 
Thrill,  systolic,  in  aortic  stenosis,  384 

in  congenital  heart  disease,  439 
in  mitral  insufficiency,  330 
Thrills,  mechanics  of,  92 
Thrombi  in  cardiac  chambers,  243 

in  mitral  stenosis,  243 
Thromboangitis  obliterans,  276 

differentiation   from   angeioneuro- 
ses,  276 
Thyreoglobulin,  576 

Thyroid  gland  changes  in  Basedow's  disease, 
585 
size  of  normal,  585 
Thyroid  heart,  574 

(hypothyroidism),  575 
formes  frustes,  574 
from  pressure,  574 
in  simple  goitre,  574 
Thyroid   secretion   (see  Hyperthyroidism), 
578 
of  thyreoglobulin  and  iodothyrin, 

576 
physiological  effects  of,  577 
relation  to  histological  structure, 
576 
Thyroidectin,  588 
Thyroidectomy,  589 
Tobacco  angina,  293 
Tobacco,  effect  of,  on  circulation,  610 

on  coronary  circulation,  611 
"Tobacco  heart,"  609 
Tobacco,  precordial  pain  from,  610 

prohibition  of,  169 
Tobacco  smoke,  composition  of,  609 
Tonicity,  effect  of  digitalis  on,  176 

effect  of,  on  cardiac  overstrain,  135 

effect  of,  on  residual  blood,  135 

factors  producing  changes  in,  13 

of  the  cardiac  muscle,  11 

of    the  heart    in   mitral   insufficiency, 

328 
of  the  right  ventricle,  34 
Tonograph,  22 
Tonsillectomy  in  endocarditis,  317 

in  mitral  insufficiency,  337 
Tonsillitis  as  cause  of  Basedow's  disease, 

580 
Tonus  (see  Tonicity) 
Tortuous  arteries,  260 

Tracheal    percussion    shock    in   aneurism, 
533 
tug  in  aneurism,  533 
Training  at  end  of  treatment,  199 

effect  of,  130 
Trauma  as  cause  of  thoracic  aneurism,  526 
cardiac,  513 


INDEX. 


631 


Trauma,  lesions  due  to,  519 

of  heart,  518 
Treatment  of  heart  failure,  general  princi- 
ples, 163 
relation  of,  to  occupation,  199 
Tricuspid  area,  102 

Tricuspid     insufficiency,     arrhythmia      in 
cases  of,  402 
diagnosis  of,  404 
effect  on  circulation,  397 
functional,  396 

in  paroxysmal  tachycardia,  568 
organic,  396 

pathological  physiology,  397 
symptoms  of,  399 
systolic  murmur  in,  400 
treatment  of,  404 
variations  in  murmur,  401 
venous  pulse  in,  398 
Tricuspid  stenosis,  406 

cyanosis  in,  408 
effect  on  the  circulation,  407 
etiology  of,  406 
occurrence  of,  406 
pathology  of,  407 
presystolic  rumble  in,  409 
pulmonary  infarction  in,  409 
treatment  of,  411 
Tricuspid  valve,  demonstration  of  action  of, 
10 
malformation  of,  458 
opening  of,  55 
Trigeminal  pulse,  72 
Truncus  arteriosus,  422 
division  of,  425 
Tuberculosis  as  cause  of  endocarditis,  303 
in  persons  with  mitral  stenosis,  342 
in  pulmonary  stenosis,  440 
of  the  heart,  244 
Tumors  of  the  heart,  245 

hsemopericardium  from,  246 
Typhoid  fever  as  cause  of  Basedow's  disease, 
580 
blood-pressure  in,  31 


Uraemia,  blood-pressure  in,  28,  29 
Urine,  albumin  and  casts  in,  156 

amount  of  in  cardiac  disease,  156 
chloride  metabohsm  in,  156 


Vagus  currents,  with  heart-beat,  157 

with  respiration,  157 
Vagus  effect  in  producing  heart-block,  461 
Valve,    Eustachian    (of   the   inferior   vena 

cava),  424 
Valves,  auriculoventricular,  diastolic  closure 
of,  56 
in  veins,  closure  of,  50 


Valves,  movements  of,  8 

position  of,  in  diastole,  10 
Valvular  areas  in  auscultation,  102 
Vasa  vasorum,  changes  in,  in  arteriosclero- 
sis, 250 
Vascular  crises,  blood-pressure  in,  30 
Vasomotor  angina,  291 
Vasomotor  crises,  270 

hypotensive,  274 
use  of  nitrites  in,  270 
Veins,  cardinal,  422 
sounds  over,  118 

umbiUcal  (omphalomesaraic),  422 
visible  pulsations  in,  49 
vitelline,  422 
Venesection,  165 

contraindications  to,  166 

effect  of,  in  hypertension  of  intracranial 

origin,  30 
effect  of,  on  the  circulation,  166 
in  arteriosclerosis,  266 
technique  of,  165 
Veno-auricular  junction,  anatomy  of,  5 
Venous  pressure,  141 

determination  of,  32 
effect  of,  on  filling  of  the  heart,  11 
in  broken  compensation,  141 
in  neurasthenics,  593 
in  paroxysmal  tachycardia,  566 
Venous  pulse,  49 

diastolic,  56 

double,  49 

in  auricular  paralysis,  57 

in  paroxysmal  tachycardia,  561 

information  furnished  by,  58 

negative,  49 

physiological,  49 

positive,  57 

presystolic,  56 

relation  to  atmospheric  pressure, 

50 
technique  of  tracings,  50 
visual  examination  of,  56 
Venous  tracing,  interpretation  of,  53 
Ventricle,  left,  pressure  within,  18 
Ventricle,  third,  432 
Ventricles,  filling  of,  9 
Ventricular  muscle,  anatomy  of,  8 
Viscosity  of  the  blood,  38 

apparatus  for  clinical  determina- 
tion of,  38 
factors  influencing,  38,  39 
diet,  39 
hydraemia,  39 
number  of  red  blood-cells, 
39 
Volume  curve,  method  of  recording,  9 
Vomiting,  blood -pressure  in,  32 
Von   Graefe's   sign   in   Basedow's    disease, 
583 


632 


INDEX. 


Walking  in  treatment  of  heart  lesions,  197 

regulation  of  speed  and  respiration,  198 
Water-hammer  pulse,  47 
Weather,  effect  of,  on  cardiac  symptoms,  147 
Whiskey  in  cardiac  disease,  168 
Wiring  treatment  of  aneurism,  552 
Work  of  the  heart,  26 
Worry,  effect  of,  on  circulation,  612 
Wounds  of  the  heart,  513 

control  of  hemorrhage  from, 
517 

results  of  operation,  518 

suture  of,  516 
Wrestling,  effect  of,  on  the  heart,  133 


Xiphisternal  line  as  sign  of  level  of  dia- 
phragm, 598 
X-ray,  cardiac  shadow,  83 

examination  in  oblique  axes,  84 
of  adherent  pericardium,  507 
of  sclerotic  arteries,  260 
magnification  of  shadow,  82 
methods  of  examination,  82 
oblique  illuminations,  83 
pulmonary  shadows,  83 
shadow  in  aneurism,  536 


Zander  exercises,  197 


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